[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 5620
1. Rezze GG, Leon A, Duprat J: Dysplastic nevus (atypical nevus). An Bras Dermatol; 2010 Nov-Dec;85(6):863-71
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dysplastic nevus (atypical nevus).
  • Atypical nevum (dysplastic) is considered an important factor associated with increased risk of developing cutaneous melanoma.
  • It is believed that atypical nevi are precursor lesions of cutaneous melanoma.
  • They may be present in patients with multiple melanocytic nevi (atypical nevus syndrome) or isolated and in small numbers in a non-familial context.
  • The major challenge in relation to atypical nevi lies in the controversy of defining its nomenclature, clinical diagnosis, dermoscopic criteria, histopathological diagnosis and molecular aspects.
  • This review aims at bringing knowledge, facilitating comprehension and clarifying doubts about atypical nevus.
  • [MeSH-major] Dysplastic Nevus Syndrome / pathology. Melanoma / pathology. Precancerous Conditions / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Dermoscopy. Diagnosis, Differential. Humans

  • Genetic Alliance. consumer health - Nevus.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] An Bras Dermatol. 2011 Feb;86(1):182
  • (PMID = 21308311.001).
  • [ISSN] 1806-4841
  • [Journal-full-title] Anais brasileiros de dermatologia
  • [ISO-abbreviation] An Bras Dermatol
  • [Language] eng; por
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  •  go-up   go-down


2. de Snoo FA, Hottenga JJ, Gillanders EM, Sandkuijl LA, Jones MP, Bergman W, van der Drift C, van Leeuwen I, van Mourik L, Huurne JA, Frants RR, Willemze R, Breuning MH, Trent JM, Gruis NA: Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families. Eur J Hum Genet; 2008 Sep;16(9):1135-41
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families.
  • However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers.
  • The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma.
  • The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score=2.751), a region containing candidate gene CDK6.
  • [MeSH-major] Dysplastic Nevus Syndrome / genetics. Genes, p16. Genetic Linkage / genetics. Melanoma / genetics. Skin Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18398432.001).
  • [ISSN] 1018-4813
  • [Journal-full-title] European journal of human genetics : EJHG
  • [ISO-abbreviation] Eur. J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 6
  •  go-up   go-down


3. Schäfer T, Merkl J, Klemm E, Wichmann HE, Ring J, KORA Study Group: The epidemiology of nevi and signs of skin aging in the adult general population: Results of the KORA-survey 2000. J Invest Dermatol; 2006 Jul;126(7):1490-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The epidemiology of nevi and signs of skin aging in the adult general population: Results of the KORA-survey 2000.
  • Nevi can approximate the melanoma risk and demographic changes will increase the meaning of signs of skin aging (SSA).
  • However, little is known about the epidemiology of nevi and SSA in the general adult population.
  • We aimed to estimate the prevalence and age distribution of common and atypical nevi and SSA as well as gender differences in a large population-based sample.
  • Most subjects (60.3%) exhibited 11 to 50 common nevi and 5.2% had at least one atypical nevus.
  • All signs of skin aging increased significantly with age and so did lentigines solaris, seniles, and actinic keratoses.
  • In contrast, common and atypical nevi and ephelides decreased significantly with age.
  • Signs of skin aging are frequent and increase, in contrast to common and atypical nevi, with age.
  • [MeSH-major] Nevus / epidemiology. Nevus / pathology. Skin Aging / pathology. Skin Neoplasms / epidemiology. Skin Neoplasms / pathology


Advertisement
4. King R, Page RN, Googe PB, Mihm MC Jr: Lentiginous melanoma: a histologic pattern of melanoma to be distinguished from lentiginous nevus. Mod Pathol; 2005 Oct;18(10):1397-401
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lentiginous melanoma: a histologic pattern of melanoma to be distinguished from lentiginous nevus.
  • Atypical lentiginous melanocytic proliferations in elderly patients continue to pose a diagnostic dilemma with lesions variably categorized as dysplastic nevus, atypical junctional nevus, melanoma in situ (early or evolving) and premalignant melanosis.
  • The clinical diagnosis was variable and included lentigo maligna, atypical nevus, pigmented basal cell carcinoma, seborrheic keratosis and lentigo.
  • The initial biopsies mimicked lentiginous nevus or dysplastic nevus and were characterized by a lentiginous proliferation of melanocytes at the dermoepidermal junction both as single cells and as small nests with areas of confluent growth, extending to the edges of the biopsy.
  • The retiform epidermis was maintained and pagetoid spread of melanocytes was not prominent in hematoxylin- and eosin- stained sections.
  • Dermal fibrosis was variably present and the melanocytic proliferation demonstrated cytological atypia.
  • The subsequent re-excisions demonstrated similar atypical melanocytic proliferation occurring over a broad area flanking the prior biopsy sites.
  • The diagnosis of melanoma was more easily recognized in the complete excision specimens.
  • Immunohistochemical stains for Mitf and Mart-1 highlighted the extent of the basalar melanocytic proliferation as well as foci of pagetoid spread by melanocytes.
  • Familiarity with this pattern of early melanoma should facilitate proper classification of lentiginous melanocytic proliferations in biopsies from older adults.
  • [MeSH-major] Dysplastic Nevus Syndrome / diagnosis. Hutchinson's Melanotic Freckle / diagnosis. Lentigo / diagnosis. Melanoma / diagnosis. Nevus, Pigmented / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged

  • Genetic Alliance. consumer health - Nevus.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15976811.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


5. Penberthy WT, Tsunoda I: The importance of NAD in multiple sclerosis. Curr Pharm Des; 2009;15(1):64-99
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The importance of NAD in multiple sclerosis.
  • During chronic CNS inflammation, nicotinamide adenine dinucleotide (NAD) concentrations are altered by (T helper) Th1-derived cytokines through the coordinated induction of both indoleamine 2,3-dioxygenase (IDO) and the ADP cyclase CD38 in pathogenic microglia and lymphocytes.
  • While IDO activation may keep auto-reactive T cells in check, hyper-activation of IDO can leave neuronal CNS cells starving for extracellular sources of NAD.
  • Existing data indicate that glia may serve critical functions as an essential supplier of NAD to neurons during times of stress.
  • Administration of pharmacological doses of non-tryptophan NAD precursors ameliorates pathogenesis in animal models of MS.
  • This resistance is due to increased efficiency of NAD biosynthesis that delays stress-induced depletion of axonal NAD and ATP.
  • In this review, we contrast the role of NAD in EAE versus TMEV demyelinating pathogenesis to increase our understanding of the pharmacotherapeutic potential of NAD signal transduction pathways.
  • A comprehensive review of immunomodulatory control of NAD biosynthesis and degradation in MS pathogenesis is presented.
  • Distinctive pharmacological approaches designed for NAD-complementation or targeting NAD-centric proteins (SIRT1, SIRT2, PARP-1, GPR109a, and CD38) are outlined towards determining which approach may work best in the context of clinical application.

  • Genetic Alliance. consumer health - Multiple Sclerosis.
  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Lancet. 2007 Aug 4;370(9585):389-97 [17679016.001]
  • [Cites] Oncogene. 2007 Aug 13;26(37):5505-20 [17694090.001]
  • [Cites] Br J Dermatol. 2007 Sep;157(3):540-6 [17596147.001]
  • [Cites] J Biol Chem. 2007 Aug 24;282(34):24574-82 [17604275.001]
  • [Cites] N Engl J Med. 2007 Aug 30;357(9):927-9 [17660531.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2570-82 [17710230.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Nov 3;362(4):946-50 [17803959.001]
  • [Cites] Nat Rev Immunol. 2007 Oct;7(10):817-23 [17767193.001]
  • [Cites] Regen Med. 2007 Sep;2(5):817-29 [17907933.001]
  • [Cites] Cardiovasc Drug Rev. 2007 Fall;25(3):235-60 [17919258.001]
  • [Cites] Med Sci (Paris). 2007 Oct;23(10):840-4 [17937892.001]
  • [Cites] Mol Cell Biol. 2007 Nov;27(21):7475-85 [17785446.001]
  • [Cites] Cell Mol Life Sci. 2007 Oct;64(19-20):2542-63 [17611712.001]
  • [Cites] FASEB J. 2007 Nov;21(13):3629-39 [17585054.001]
  • [Cites] PLoS Biol. 2007 Oct 2;5(10):e263 [17914902.001]
  • [Cites] PLoS Biol. 2007 Oct;5(10):e257 [17896864.001]
  • [Cites] Am J Pathol. 2007 Nov;171(5):1563-75 [17823280.001]
  • [Cites] Cell Metab. 2007 Nov;6(5):363-75 [17983582.001]
  • [Cites] J Immunol. 2007 Dec 1;179(11):7827-39 [18025229.001]
  • [Cites] Mol Pharmacol. 2007 Dec;72(6):1508-21 [17872969.001]
  • [Cites] J Neurosci. 2007 Nov 21;27(47):12884-92 [18032661.001]
  • [Cites] J Neuroimmune Pharmacol. 2007 Sep;2(3):270-5 [18040861.001]
  • [Cites] Mol Cell Biol. 2007 Dec;27(24):8807-14 [17923681.001]
  • [Cites] Mol Cell Biol. 2008 Jan;28(1):30-9 [17954562.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Feb 1;366(1):174-9 [18054327.001]
  • [Cites] PLoS One. 2007;2(12):e1331 [18159229.001]
  • [Cites] J Biol Chem. 2008 Jan 4;283(1):202-12 [17981805.001]
  • [Cites] Life Sci. 2008 Jan 16;82(3-4):205-9 [18078960.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2008;48:79-106 [17705685.001]
  • [Cites] Immunol Lett. 2008 Jan 29;115(2):153-9 [18082271.001]
  • [Cites] J Neuroimmunol. 2008 Jan;193(1-2):12-23 [18077006.001]
  • [Cites] J Biomol Screen. 2008 Jan;13(1):54-61 [18057180.001]
  • [Cites] Nat Rev Drug Discov. 2008 Feb;7(2):143-55 [18239670.001]
  • [Cites] Neurochem Int. 2008 Mar-Apr;52(4-5):751-60 [18029056.001]
  • [Cites] Free Radic Biol Med. 2008 Feb 15;44(4):527-37 [17997992.001]
  • [Cites] Int J Cardiol. 2008 Feb 29;124(2):172-8 [17395297.001]
  • [Cites] Cell Metab. 2008 Feb;7(2):104-12 [18249170.001]
  • [Cites] Cell Motil Cytoskeleton. 2008 Mar;65(3):179-82 [18044719.001]
  • [Cites] Brain. 2008 Mar;131(Pt 3):785-99 [18156156.001]
  • [Cites] Nat Clin Pract Rheumatol. 2008 Mar;4(3):136-44 [18200008.001]
  • [Cites] Autophagy. 2008 Apr;4(3):286-9 [18094610.001]
  • [Cites] Biochem J. 2008 Apr 1;411(1):63-70 [18215126.001]
  • [Cites] Biochem J. 2008 Apr 1;411(1):e1-3 [18333834.001]
  • [Cites] PLoS One. 2008;3(3):e1759 [18335035.001]
  • [Cites] Biochem J. 2008 Apr 15;411(2):279-85 [18215119.001]
  • [Cites] J Leukoc Biol. 2008 Apr;83(4):804-16 [18252866.001]
  • [Cites] Cell Stem Cell. 2007 Aug 16;1(2):135-6 [18371345.001]
  • [Cites] Cell Stem Cell. 2008 Mar 6;2(3):241-51 [18371449.001]
  • [Cites] Am J Cardiol. 2008 Apr 17;101(8A):20B-26B [18375237.001]
  • [Cites] Neurochem Int. 2008 May;52(6):1297-303 [18328600.001]
  • [Cites] Nat Cell Biol. 2008 Apr;10(4):385-94 [18344989.001]
  • [Cites] Nat Cell Biol. 2008 Apr;10(4):373-4 [18379594.001]
  • [Cites] Neuron. 2008 Apr 10;58(1):10-4 [18400158.001]
  • [Cites] Mol Cell Biol. 2008 May;28(9):2860-71 [18299389.001]
  • [Cites] Arch Neurol. 2008 Apr;65(4):452-6 [18413466.001]
  • [Cites] Cancer Biol Ther. 2007 Dec;6(12):1833-6 [18087218.001]
  • [Cites] Curr Opin Neurol. 2008 Jun;21(3):242-7 [18451705.001]
  • [Cites] Exp Neurol. 2008 May;211(1):214-26 [18346732.001]
  • [Cites] Nutr Rev. 2008 May;66(5):250-5 [18454811.001]
  • [Cites] Pharmacol Res. 2008 Apr;57(4):318-23 [18434188.001]
  • [Cites] Br J Pharmacol. 2002 Nov;137(6):761-70 [12411406.001]
  • [Cites] Springer Semin Immunopathol. 2002;24(2):105-25 [12503060.001]
  • [Cites] Toxicology. 2002 Dec 27;181-182:65-70 [12505286.001]
  • [Cites] Brain Pathol. 2003 Jan;13(1):23-33 [12580542.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):366-74 [12590258.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):327-8 [12610543.001]
  • [Cites] Nat Med. 2003 Mar;9(3):352-5 [12563315.001]
  • [Cites] Nature. 2003 Apr 17;422(6933):688-94 [12700753.001]
  • [Cites] Trends Pharmacol Sci. 2003 May;24(5):228-32 [12767721.001]
  • [Cites] J Immunol. 2003 Sep 15;171(6):2863-72 [12960308.001]
  • [Cites] Biochem Pharmacol. 2003 Sep 15;66(6):1033-6 [12963490.001]
  • [Cites] Nature. 2003 Sep 11;425(6954):191-6 [12939617.001]
  • [Cites] Nat Med. 2003 Oct;9(10):1269-74 [14502282.001]
  • [Cites] Cell Mol Life Sci. 2003 Sep;60(9):1990-7 [14523559.001]
  • [Cites] J Virol. 2003 Nov;77(22):12252-65 [14581562.001]
  • [Cites] J Immunol. 2004 Feb 1;172(3):1896-906 [14734775.001]
  • [Cites] Mult Scler. 2004 Feb;10(1):26-34 [14760949.001]
  • [Cites] J Virol. 2004 Mar;78(5):2632-6 [14963171.001]
  • [Cites] J Neuroimmunol. 2004 Mar;148(1-2):116-26 [14975592.001]
  • [Cites] J Immunol. 2004 Apr 1;172(7):4100-10 [15034022.001]
  • [Cites] Biochem Pharmacol. 2004 Feb 1;67(3):411-9 [15037193.001]
  • [Cites] Neurobiol Dis. 2004 Apr;15(3):618-29 [15056470.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18895-902 [14960594.001]
  • [Cites] Cell. 2004 May 14;117(4):495-502 [15137942.001]
  • [Cites] Adv Exp Med Biol. 2003;527:113-8 [15206723.001]
  • [Cites] J Cereb Blood Flow Metab. 2004 Jul;24(7):728-43 [15241181.001]
  • [Cites] Mol Microbiol. 2004 Aug;53(4):1003-9 [15306006.001]
  • [Cites] Science. 2004 Aug 13;305(5686):1010-3 [15310905.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Sep;310(3):1053-61 [15159442.001]
  • [Cites] Nutrition. 2004 Sep;20(9):778-82 [15325687.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2500-20 [15353303.001]
  • [Cites] Physiol Rev. 2007 Jan;87(1):245-313 [17237347.001]
  • [Cites] J Neuroinflammation. 2007;4:6 [17254325.001]
  • [Cites] Neurochem Res. 2007 Feb;32(2):187-95 [16933150.001]
  • [Cites] Mult Scler. 2007 Jan;13(1):33-40 [17294609.001]
  • [Cites] Neuroscience. 2007 Mar 2;145(1):11-9 [17218064.001]
  • [Cites] J Neurosci. 2007 Feb 21;27(8):1933-41 [17314289.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6823-32 [17197703.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1351-6 [17322921.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 20;355(4):1075-80 [17335774.001]
  • [Cites] Ann Neurol. 2007 Mar;61(3):209-18 [17187374.001]
  • [Cites] Ann Neurol. 2007 Mar;61(3):219-27 [17387730.001]
  • [Cites] Curr Drug Metab. 2007 Apr;8(3):197-200 [17430106.001]
  • [Cites] Curr Drug Metab. 2007 Apr;8(3):245-66 [17430113.001]
  • [Cites] Genes Dev. 2007 Apr 15;21(8):920-8 [17437997.001]
  • [Cites] Autoimmunity. 2007 Mar;40(2):148-60 [17453713.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1695-712 [17456775.001]
  • [Cites] Eur J Immunol. 2007 May;37(5):1290-301 [17407101.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 24;104(17):7217-22 [17438283.001]
  • [Cites] Expert Opin Ther Targets. 2007 May;11(5):695-705 [17465726.001]
  • [Cites] Nat Med. 2007 May;13(5):579-86 [17417651.001]
  • [Cites] Brain Pathol. 2007 Jan;17(1):45-55 [17493037.001]
  • [Cites] Gene. 2007 Jul 1;396(1):203-13 [17499941.001]
  • [Cites] Diabetologia. 2007 Jul;50(7):1523-31 [17508197.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Aug 3;359(3):665-71 [17560549.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):305-12 [17579050.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):1007-11 [17581586.001]
  • [Cites] Neurochem Int. 2007 Jun;50(7-8):954-8 [17222947.001]
  • [Cites] Med Hypotheses. 2007;69(3):618-28 [17349750.001]
  • [Cites] Expert Rev Mol Med. 2007;9(20):1-19 [17637110.001]
  • [Cites] J Neurosci. 2007 Jul 18;27(29):7717-30 [17634366.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3602-9 [17652729.001]
  • [Cites] Glia. 2007 Sep;55(12):1251-62 [17659524.001]
  • [Cites] Glia. 2007 Sep;55(12):1280-6 [17659530.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jul 21;346(1):188-92 [16750163.001]
  • [Cites] J Immunol. 2006 Jul 1;177(1):130-7 [16785507.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 20;103(25):9685-90 [16769901.001]
  • [Cites] Blood. 2006 Jul 1;108(1):228-37 [16522817.001]
  • [Cites] Diabetes Metab Res Rev. 2006 Jul-Aug;22(4):284-94 [16544364.001]
  • [Cites] Free Radic Biol Med. 2006 Jul 15;41(2):311-7 [16814112.001]
  • [Cites] J Neurosci. 2006 Aug 16;26(33):8484-91 [16914673.001]
  • [Cites] Curr Neurovasc Res. 2006 Aug;3(3):203-13 [16918384.001]
  • [Cites] Expert Rev Mol Med. 2006;8(20):1-27 [16942634.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2006 Oct;291(4):H1545-53 [16632544.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Oct 20;349(2):533-9 [16956582.001]
  • [Cites] J Neurochem. 2006 Oct;99(1):165-76 [16987244.001]
  • [Cites] J Neurosci. 2006 Sep 20;26(38):9794-804 [16988050.001]
  • [Cites] Dev Biol. 2006 Oct 1;298(1):118-31 [16875686.001]
  • [Cites] J Immunol. 2006 Oct 15;177(8):5639-46 [17015752.001]
  • [Cites] Nat Biotechnol. 2006 Oct;24(10):1179-80 [17033640.001]
  • [Cites] Eur J Neurosci. 2006 Oct;24(8):2169-76 [17042794.001]
  • [Cites] Front Biosci. 2007;12:2728-34 [17127275.001]
  • [Cites] J Neurosci. 2006 Dec 13;26(50):12904-13 [17167081.001]
  • [Cites] J Antimicrob Chemother. 2007 Jan;59(1):74-9 [17079237.001]
  • [Cites] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163.001]
  • [Cites] J Immunol. 2007 Jan 1;178(1):95-102 [17182544.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jan;320(1):458-64 [17021258.001]
  • [Cites] Adv Exp Med Biol. 2007;590:171-83 [17191385.001]
  • [Cites] Am J Pathol. 2007 Jan;170(1):214-26 [17200195.001]
  • [Cites] Trends Biochem Sci. 2007 Jan;32(1):12-9 [17161604.001]
  • [Cites] Arch Biochem Biophys. 1999 Dec 1;372(1):1-7 [10562410.001]
  • [Cites] Am Heart J. 1999 Dec;138(6 Pt 1):1082-7 [10577438.001]
  • [Cites] J Cell Biol. 1999 Dec 13;147(6):1123-8 [10601327.001]
  • [Cites] Neurosci Lett. 2000 Mar 10;281(2-3):111-4 [10704755.001]
  • [Cites] Eur J Biochem. 2000 Mar;267(6):1550-64 [10712584.001]
  • [Cites] Am J Public Health. 2000 May;90(5):727-38 [10800421.001]
  • [Cites] Development. 2000 Jun;127(12):2653-62 [10821763.001]
  • [Cites] Biochim Biophys Acta. 2000 Jun 26;1486(1):84-96 [10856715.001]
  • [Cites] Mutat Res. 2000 Jun 30;460(1):1-15 [10856830.001]
  • [Cites] Brain Pathol. 2000 Jul;10(3):402-18 [10885659.001]
  • [Cites] J Neurobiol. 2000 Jul;44(1):7-19 [10880128.001]
  • [Cites] Redox Rep. 2000;5(2-3):101-4 [10939283.001]
  • [Cites] Cancer. 2000 Aug 15;89(4):925-31 [10951359.001]
  • [Cites] N Engl J Med. 2000 Sep 28;343(13):898-904 [11006365.001]
  • [Cites] N Engl J Med. 2000 Sep 28;343(13):938-52 [11006371.001]
  • [Cites] Science. 2000 Sep 22;289(5487):2126-8 [11000115.001]
  • [Cites] Rheumatology (Oxford). 2001 Mar;40(3):329-35 [11285382.001]
  • [Cites] J Neuroimmunol. 2001 Jul 2;117(1-2):78-86 [11431007.001]
  • [Cites] Neuropediatrics. 2000 Dec;31(6):314-7 [11508552.001]
  • [Cites] Cell. 2001 Oct 19;107(2):149-59 [11672523.001]
  • [Cites] Science. 2001 Nov 9;294(5545):1296-7 [11701918.001]
  • [Cites] Nat Neurosci. 2001 Dec;4(12):1199-206 [11770485.001]
  • [Cites] Mol Med. 2001 Nov;7(11):761-6 [11788790.001]
  • [Cites] Infect Immun. 2002 Feb;70(2):859-68 [11796621.001]
  • [Cites] Free Radic Biol Med. 2002 Feb 15;32(4):314-8 [11841921.001]
  • [Cites] J Immunol. 2002 Mar 1;168(5):2508-15 [11859145.001]
  • [Cites] Herpes. 2001 Nov;8(3):60-3 [11867021.001]
  • [Cites] Neuroreport. 2002 Feb 11;13(2):213-6 [11893912.001]
  • [Cites] Br J Nutr. 2002 Feb;87(2):115-9 [11895163.001]
  • [Cites] Brain. 2002 Jun;125(Pt 6):1297-308 [12023318.001]
  • [Cites] CNS Drugs. 2002;16(6):405-18 [12027786.001]
  • [Cites] Neuropsychopharmacology. 2002 Aug;27(2):309-18 [12093605.001]
  • [Cites] Arch Immunol Ther Exp (Warsz). 2002;50(3):187-96 [12098934.001]
  • [Cites] J Neuroimmunol. 2002 Aug;129(1-2):186-96 [12161035.001]
  • [Cites] Pharmacol Biochem Behav. 2002 Nov;73(4):901-10 [12213537.001]
  • [Cites] Trends Neurosci. 2002 Oct;25(10):532-7 [12220882.001]
  • [Cites] Pharmacol Rev. 2002 Sep;54(3):375-429 [12223530.001]
  • [Cites] Mol Med. 2002 May;8(5):283-9 [12359959.001]
  • [Cites] J Neuroimmunol. 2008 Jul 15;197(2):140-6 [18555539.001]
  • [Cites] Physiol Rev. 2008 Jul;88(3):841-86 [18626062.001]
  • [Cites] Biosci Biotechnol Biochem. 2008 Jul;72(7):1667-72 [18603814.001]
  • [Cites] Annu Rev Nutr. 2008;28:115-30 [18429699.001]
  • [Cites] Biochem Pharmacol. 2008 Aug 15;76(4):443-52 [18547543.001]
  • [Cites] Free Radic Biol Med. 2008 Sep 1;45(5):726-31 [18554520.001]
  • [Cites] J Biol Chem. 2008 Sep 5;283(36):24571-83 [18599483.001]
  • [Cites] Cell Cycle. 2008 Sep 15;7(18):2821-5 [18797187.001]
  • [Cites] Exp Cell Res. 2008 Oct 1;314(16):3069-74 [18687325.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14447-52 [18794531.001]
  • [Cites] Phytother Res. 2008 Oct;22(10):1367-71 [18688788.001]
  • [Cites] J Leukoc Biol. 2008 Oct;84(4):940-8 [18678605.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6384-401 [18710944.001]
  • [Cites] J Cell Biochem. 2008 Oct 15;105(3):905-12 [18759251.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15599-604 [18829436.001]
  • [Cites] J Nutr Biochem. 2008 Nov;19(11):746-53 [18436439.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2008 Nov;28(11):2016-22 [18669886.001]
  • [Cites] Brain. 2008 Nov;131(Pt 11):3081-91 [18790823.001]
  • [Cites] Atherosclerosis. 2009 Jan;202(1):68-75 [18550065.001]
  • [Cites] Int J Biochem Cell Biol. 2009 Mar;41(3):467-71 [18282734.001]
  • [Cites] Cardiovasc Res. 2009 Feb 15;81(3):582-91 [18719074.001]
  • [Cites] Cell Metab. 2008 May;7(5):365-75 [18460328.001]
  • [Cites] J Neurosci Res. 2005 Apr 1;80(1):66-74 [15723383.001]
  • [Cites] Brain Res. 2005 May 17;1044(1):8-15 [15862784.001]
  • [Cites] Nat Rev Drug Discov. 2005 May;4(5):421-40 [15864271.001]
  • [Cites] Methods. 2005 Jun;36(2):117-28 [15893938.001]
  • [Cites] J Clin Invest. 2005 Jun;115(6):1449-57 [15931380.001]
  • [Cites] J Neurol Sci. 2005 Jun 15;233(1-2):93-7 [15896807.001]
  • [Cites] J Physiol Biochem. 2004 Dec;60(4):245-52 [15957242.001]
  • [Cites] Shock. 2005 Jul;24(1):59-65 [15988322.001]
  • [Cites] J Neurosci Res. 2005 Jul 1;81(1):1-8 [15920740.001]
  • [Cites] J Neurosci Res. 2005 Jul 15;81(2):190-8 [15931673.001]
  • [Cites] J Neuroimmunol. 2005 Aug;165(1-2):83-91 [15958276.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):266-71 [16015332.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26649-52 [15929991.001]
  • [Cites] FASEB J. 2005 Aug;19(10):1347-9 [15939737.001]
  • [Cites] J Cell Biol. 2005 Aug 1;170(3):349-55 [16043516.001]
  • [Cites] Neuroscientist. 2005 Aug;11(4):308-22 [16061518.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1755-61 [15905186.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):3075-83 [16116196.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2375-81 [15947091.001]
  • [Cites] Curr Neurovasc Res. 2005 Oct;2(4):271-85 [16181120.001]
  • [Cites] Mol Biol Cell. 2005 Oct;16(10):4623-35 [16079181.001]
  • [Cites] Neurotoxicology. 2005 Oct;26(5):847-55 [15923038.001]
  • [Cites] Nat Clin Pract Cardiovasc Med. 2004 Dec;1(2):84-9 [16265311.001]
  • [Cites] Science. 2005 Nov 4;310(5749):850-5 [16272121.001]
  • [Cites] Inflamm Res. 2005 Nov;54(11):435-50 [16307217.001]
  • [Cites] J Clin Invest. 2005 Dec;115(12):3634-40 [16322797.001]
  • [Cites] J Biol Chem. 2005 Dec 30;280(52):43121-30 [16207712.001]
  • [Cites] Adv Neurol. 2006;98:77-89 [16400828.001]
  • [Cites] Clin Chim Acta. 2006 Feb;364(1-2):82-90 [16139256.001]
  • [Cites] Biochem Pharmacol. 2006 Feb 28;71(5):646-56 [16386710.001]
  • [Cites] Hum Mol Genet. 2006 Feb 15;15(4):625-35 [16403805.001]
  • [Cites] Int J Cardiol. 2006 Apr 4;108(2):143-54 [15978685.001]
  • [Cites] No To Shinkei. 2006 Feb;58(2):141-4 [16519110.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Apr 21;342(4):1312-8 [16516847.001]
  • [Cites] Brain Res. 2006 Feb 16;1073-1074:25-37 [16448631.001]
  • [Cites] Blood. 2006 Apr 1;107(7):2846-54 [16339401.001]
  • [Cites] Curr Med Chem. 2006;13(8):967-77 [16611078.001]
  • [Cites] Cell Cycle. 2006 Apr;5(8):873-7 [16628003.001]
  • [Cites] Ann Pharmacother. 2006 Jun;40(6):1158-61 [16684809.001]
  • [Cites] Nat Rev Drug Discov. 2006 Jun;5(6):493-506 [16732220.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jul 14;345(4):1386-92 [16730329.001]
  • [Cites] Neuron. 2006 Jun 15;50(6):819-21 [16772165.001]
  • [Cites] Int J Dermatol. 1983 Jan-Feb;22(1):44-5 [6832880.001]
  • [Cites] Biochemistry. 1983 Oct 25;22(22):5188-94 [6317018.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Feb;81(3):908-12 [6422465.001]
  • [Cites] J Clin Invest. 1986 Apr;77(4):1312-20 [2937805.001]
  • [Cites] Infect Immun. 1986 Aug;53(2):347-51 [3089936.001]
  • [Cites] Lancet. 1987 Apr 18;1(8538):893-5 [2882294.001]
  • [Cites] Neurology. 1987 Jul;37(7):1097-102 [3110648.001]
  • [Cites] Int J Tissue React. 1987;9(4):317-24 [3114164.001]
  • [Cites] Lancet. 1987 Oct 17;2(8564):920 [2889118.001]
  • [Cites] J Neuroimmunol. 1989 Dec;25(2-3):151-9 [2685040.001]
  • [Cites] Postgrad Med. 1990 Jan;87(1):163-7, 170 [2296564.001]
  • [Cites] N Engl J Med. 1990 Mar 29;322(13):874-81 [1690352.001]
  • [Cites] Arch Biochem Biophys. 1990 Nov 15;283(1):40-5 [2146924.001]
  • [Cites] J Neurocytol. 1990 Aug;19(4):494-503 [1700810.001]
  • [Cites] Acta Neuropathol. 1990;80(5):521-6 [2251909.001]
  • [Cites] J Neurosci. 1991 Oct;11(10):3146-54 [1941078.001]
  • [Cites] Adv Exp Med Biol. 1991;294:675-8 [1837697.001]
  • [Cites] J Neurol Sci. 1992 Jun;109(2):140-7 [1634896.001]
  • [Cites] J Neuroimmunol. 1992 Oct;40(2-3):225-30 [1430153.001]
  • [Cites] Br J Dermatol. 1993 May;128(5):578-80 [8504053.001]
  • [Cites] J Am Coll Nutr. 1993 Aug;12(4):412-6 [8409103.001]
  • [Cites] J Neurosci. 1993 Oct;13(10):4354-60 [8410191.001]
  • [Cites] Science. 1993 Oct 29;262(5134):695-700 [8235590.001]
  • [Cites] J Neurol. 1993 Dec;241(2):108-14 [8138825.001]
  • [Cites] J Neurosci. 1994 Jun;14(6):3915-21 [8207495.001]
  • [Cites] Intern Med. 1994 Feb;33(2):82-6 [8019047.001]
  • [Cites] J Neuropathol Exp Neurol. 1996 Jun;55(6):673-86 [8642393.001]
  • [Cites] Neurology. 1996 Apr;46(4):907-11 [8780061.001]
  • [Cites] Neurology. 1996 Sep;47(3):829-34 [8797491.001]
  • [Cites] Nat Med. 1997 Jan;3(1):73-6 [8986744.001]
  • [Cites] J Nutr. 1997 Jan;127(1):117-21 [9040554.001]
  • [Cites] J Exp Med. 1997 Oct 6;186(7):1041-9 [9314553.001]
  • [Cites] Nat Med. 1997 Oct;3(10):1089-95 [9334719.001]
  • [Cites] J Cereb Blood Flow Metab. 1997 Nov;17(11):1143-51 [9390645.001]
  • [Cites] Am J Pathol. 1998 Feb;152(2):611-9 [9466588.001]
  • [Cites] J Neurochem. 1998 Apr;70(4):1759-63 [9523595.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1324-33 [9694721.001]
  • [Cites] Science. 1998 Aug 21;281(5380):1191-3 [9712583.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Aug;57(8):758-67 [9720491.001]
  • [Cites] J Infect Dis. 1998 Sep;178(3):875-8 [9728563.001]
  • [Cites] Eur J Immunol. 1998 Nov;28(11):3435-47 [9842886.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15769-74 [9861045.001]
  • [Cites] J Immunol. 1999 Jan 15;162(2):957-64 [9916720.001]
  • [Cites] Gastroenterology. 1999 Feb;116(2):335-45 [9922314.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1363-72 [10224276.001]
  • [Cites] Clin Exp Dermatol. 1999 May;24(3):167-9 [10354170.001]
  • [Cites] J Ment Sci. 1952 Jan;98(410):130-42 [14898212.001]
  • [Cites] J Clin Exp Psychopathol. 1957 Apr-Jun;18(2):131-58 [13439009.001]
  • [Cites] Lancet. 1962 Feb 10;1(7224):316-9 [14482545.001]
  • [Cites] Can Med Assoc J. 1959 Aug 15;81:235-8 [14402370.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50754-63 [15381699.001]
  • [Cites] Am J Forensic Med Pathol. 2004 Dec;25(4):342-4 [15577526.001]
  • [Cites] J Immunol. 2005 Feb 15;174(4):1971-9 [15699125.001]
  • [Cites] Nat Med. 2005 Mar;11(3):312-9 [15711557.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3748-54 [15356121.001]
  • [Cites] Toxicology. 2005 Apr 15;209(2):135-47 [15767026.001]
  • [Cites] BMC Genomics. 2008;9:171 [18412984.001]
  • [Cites] Dev Cell. 2008 May;14(5):661-73 [18477450.001]
  • [Cites] J Neuropathol Exp Neurol. 2008 Jun;67(6):543-54 [18520773.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):92-103 [18566373.001]
  • [Cites] Autoimmunity. 2008 Aug;41(5):405-13 [18568646.001]
  • [Cites] Am J Pathol. 2008 Jul;173(1):2-13 [18535182.001]
  • [Cites] Genes Dev. 2008 Jul 1;22(13):1753-7 [18550784.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2562-73 [18568076.001]
  • [Cites] Microbes Infect. 2004 Jul;6(9):806-12 [15374002.001]
  • [Cites] Nat Rev Immunol. 2004 Oct;4(10):762-74 [15459668.001]
  • [Cites] Steroids. 2004 Sep;69(10):653-9 [15465110.001]
  • [Cites] J Endocrinol Invest. 2004 Jul-Aug;27(7):695-707 [15505998.001]
  • [Cites] Nat New Biol. 1971 Nov 10;234(45):62-4 [5288733.001]
  • [Cites] J Neural Transm. 1973;34(3):205-14 [4146521.001]
  • [Cites] Nutr Rev. 1975 Jan;33(1):15-7 [1089213.001]
  • [Cites] J Neural Transm. 1975;37(4):297-304 [1206393.001]
  • [Cites] Acta Neuropathol. 1978 Nov 15;44(2):91-102 [213928.001]
  • [Cites] J Nutr. 1979 Apr;109(4):654-62 [34678.001]
  • [Cites] J Neurochem. 1979 Oct;33(4):895-904 [158635.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1981 Mar;44(3):209-15 [7229643.001]
  • (PMID = 19149604.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R21 NS059724; United States / NINDS NIH HHS / NS / R21 NS059724-01A2; United States / NINDS NIH HHS / NS / R21NS059724
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0U46U6E8UK / NAD
  • [Number-of-references] 346
  • [Other-IDs] NLM/ NIHMS96557; NLM/ PMC2651433
  •  go-up   go-down


6. Lin H, Kwan AL, Dutcher SK: Synthesizing and salvaging NAD: lessons learned from Chlamydomonas reinhardtii. PLoS Genet; 2010 Sep 09;6(9):e1001105
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesizing and salvaging NAD: lessons learned from Chlamydomonas reinhardtii.
  • The essential coenzyme nicotinamide adenine dinucleotide (NAD+) plays important roles in metabolic reactions and cell regulation in all organisms.
  • Bacteria, fungi, plants, and animals use different pathways to synthesize NAD+.
  • Our molecular and genetic data demonstrate that in the unicellular green alga Chlamydomonas NAD+ is synthesized from aspartate (de novo synthesis), as in plants, or nicotinamide, as in mammals (salvage synthesis).
  • The de novo pathway requires five different enzymes: L-aspartate oxidase (ASO), quinolinate synthetase (QS), quinolate phosphoribosyltransferase (QPT), nicotinate/nicotinamide mononucleotide adenylyltransferase (NMNAT), and NAD+ synthetase (NS).
  • Sequence similarity searches, gene isolation and sequencing of mutant loci indicate that mutations in each enzyme result in a nicotinamide-requiring mutant phenotype in the previously isolated nic mutants.
  • NMNAT, which is also in the de novo pathway, and nicotinamide phosphoribosyltransferase (NAMPT) constitute the nicotinamide-dependent salvage pathway.
  • A mutation in NAMPT (npt1-1) has no obvious growth defect and is not nicotinamide-dependent.
  • When the de novo pathway is inactive, the salvage pathway is essential to Chlamydomonas for the synthesis of NAD+.
  • Our results suggest that Chlamydomonas is an excellent model system to study NAD+ metabolism and cell longevity.
  • [MeSH-major] Chlamydomonas reinhardtii / metabolism. NAD / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Animals. Aspartic Acid / metabolism. Base Sequence. Biological Evolution. Biosynthetic Pathways / drug effects. Biosynthetic Pathways / genetics. Gene Expression Regulation / drug effects. Gene Expression Regulation, Plant / drug effects. Genes, Plant / genetics. Mammals. Molecular Sequence Data. Mutagenesis, Insertional / drug effects. Mutation / genetics. Niacinamide / pharmacology. Nicotinamide-Nucleotide Adenylyltransferase / metabolism. Phenotype. Plant Proteins / genetics. Plant Proteins / metabolism. Pyridines / pharmacology. Time Factors. Transcription, Genetic / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genetics. 2007 Jun;176(2):913-25 [17435233.001]
  • [Cites] Plant Cell. 2008 Oct;20(10):2909-25 [18978034.001]
  • [Cites] PLoS Genet. 2006 Oct 13;2(10):e167 [17040130.001]
  • [Cites] Nature. 2008 Feb 14;451(7180):783-8 [18273011.001]
  • [Cites] Mol Biol Cell. 1998 Jun;9(6):1293-308 [9614175.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2570-80 [10521401.001]
  • [Cites] Structure. 2005 Sep;13(9):1385-96 [16154095.001]
  • [Cites] Cell. 2006 Jan 27;124(2):315-29 [16439206.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11647-52 [16868079.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1075-80 [16618798.001]
  • [Cites] J Bacteriol. 2005 Apr;187(8):2774-82 [15805524.001]
  • [Cites] Plant J. 2007 Feb;49(4):694-703 [17270012.001]
  • [Cites] Front Biosci. 2004 May 1;9:1577-86 [14977569.001]
  • [Cites] Nature. 2008 Mar 27;452(7186):492-6 [18337721.001]
  • [Cites] Cell. 2007 Sep 21;130(6):1095-107 [17889652.001]
  • [Cites] J Bacteriol. 1999 Sep;181(17):5509-11 [10464228.001]
  • [Cites] Cell. 2007 May 4;129(3):473-84 [17482543.001]
  • [Cites] Science. 2007 Oct 12;318(5848):245-50 [17932292.001]
  • [Cites] Cell Metab. 2007 Nov;6(5):363-75 [17983582.001]
  • [Cites] J Biol Chem. 2007 Apr 13;282(15):10841-5 [17307730.001]
  • [Cites] Cell Cycle. 2007 May 2;6(9):1011-8 [17457050.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):4011-9 [8196640.001]
  • [Cites] Chem Biol. 2003 Dec;10(12):1195-204 [14700627.001]
  • [Cites] J Mol Biol. 2000 Jul 21;300(4):1005-16 [10891285.001]
  • [Cites] Mol Biol Cell. 1999 Oct;10(10):3507-20 [10512883.001]
  • [Cites] Cell. 2001 Oct 19;107(2):137-48 [11672522.001]
  • [Cites] Curr Pharm Des. 2009;15(1):20-8 [19149599.001]
  • [Cites] J Mol Biol. 2007 Oct 26;373(3):755-63 [17868694.001]
  • [Cites] Cell. 2007 Sep 7;130(5):797-810 [17803904.001]
  • [Cites] Proteomics. 2004 Jun;4(6):1581-90 [15174128.001]
  • [Cites] FEMS Microbiol Rev. 2001 Jan;25(1):15-37 [11152939.001]
  • [Cites] Science. 2009 May 1;324(5927):654-7 [19286518.001]
  • [Cites] Nature. 2001 Mar 8;410(6825):227-30 [11242085.001]
  • [Cites] Cell. 1999 Dec 23;99(7):735-45 [10619427.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 18;104(38):15150-5 [17823244.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):829-33 [17213307.001]
  • [Cites] Plant Physiol. 2006 Jul;141(3):851-7 [16698895.001]
  • [Cites] Oncogene. 2007 Aug 13;26(37):5505-20 [17694090.001]
  • [Cites] Z Vererbungsl. 1959;90(1):74-82 [13660246.001]
  • [Cites] Genetics. 1965 Jun;51(6):931-45 [17248263.001]
  • [Cites] Science. 2001 Jul 20;293(5529):510-4 [11441146.001]
  • [Cites] Genetics. 2002 Jan;160(1):181-200 [11805055.001]
  • [Cites] Cell. 2004 May 14;117(4):495-502 [15137942.001]
  • [Cites] Nature. 2008 Dec 4;456(7222):599-604 [18923395.001]
  • [Cites] Genetics. 1991 Jul;128(3):549-61 [1874415.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2216-20 [8134376.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jul 5;273(2):793-8 [10873683.001]
  • [Cites] Plant Cell. 2008 Mar;20(3):502-7 [18359853.001]
  • [Cites] Genetics. 1962 May;47:531-43 [13889019.001]
  • [Cites] Trends Biochem Sci. 2007 Jan;32(1):12-9 [17161604.001]
  • [Cites] Mol Cells. 2009 Nov 30;28(5):407-15 [19936627.001]
  • [Cites] Cell Metab. 2007 Oct;6(4):280-93 [17908557.001]
  • [Cites] Bioessays. 2003 Jul;25(7):683-90 [12815723.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7705-10 [17460045.001]
  • [Cites] Plant Physiol. 2007 Jul;144(3):1508-19 [17468215.001]
  • [Cites] J Bacteriol. 1975 Dec;124(3):1615-7 [127787.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):8524-30 [11751893.001]
  • [Cites] Genes Dev. 2008 Apr 1;22(7):918-30 [18334618.001]
  • [Cites] Cell. 2008 Jul 25;134(2):317-28 [18662546.001]
  • [Cites] Science. 2009 Apr 10;324(5924):191-2 [19359572.001]
  • [Cites] Anal Biochem. 1990 Dec;191(2):396-400 [2085185.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4678-83 [12682299.001]
  • [Cites] Trends Genet. 2007 Aug;23(8):413-8 [17559965.001]
  • [Cites] Development. 2009 Nov;136(21):3637-46 [19820182.001]
  • [Cites] Science. 2000 Sep 22;289(5487):2126-8 [11000115.001]
  • [Cites] Gene. 2001 Oct 17;277(1-2):221-9 [11602359.001]
  • [Cites] J Biol Chem. 2009 Jan 2;284(1):158-64 [19001417.001]
  • [Cites] Cell. 2010 Jan 22;140(2):280-93 [20141841.001]
  • [Cites] J Cell Sci. 2009 Feb 15;122(Pt 4):489-98 [19174463.001]
  • [Cites] Mol Biol Cell. 2000 Jul;11(7):2297-313 [10888669.001]
  • [Cites] Cell. 2008 Nov 28;135(5):907-18 [19041753.001]
  • [Cites] Science. 1989 Dec 15;246(4936):1503-4 [17756009.001]
  • [Cites] Nature. 2008 Apr 17;452(7189):887-91 [18344983.001]
  • [Cites] Nature. 2009 Oct 15;461(7266):947-55 [19829375.001]
  • [Cites] PLoS Biol. 2006 Nov;4(12):e416 [17132048.001]
  • [Cites] Genetics. 2009 Nov;183(3):885-96 [19720863.001]
  • [Cites] Eukaryot Cell. 2003 Apr;2(2):362-79 [12684385.001]
  • [Cites] J Biol Chem. 2005 May 6;280(18):18326-35 [15753098.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):15998-6003 [15520384.001]
  • [Cites] Science. 2004 Jul 16;305(5682):390-2 [15205477.001]
  • [Cites] BMC Genomics. 2009;10:210 [19422688.001]
  • [Cites] Genetics. 1995 Oct;141(2):543-9 [8647391.001]
  • [Cites] Bioinformatics. 2007 Nov 1;23(21):2947-8 [17846036.001]
  • [Cites] Genetics. 1990 Dec;126(4):875-88 [1981764.001]
  • [Cites] J Hered. 1991 Jul-Aug;82(4):295-301 [1880392.001]
  • (PMID = 20838591.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM032843; United States / NIGMS NIH HHS / GM / R01 GM032843-25A2; United States / NHGRI NIH HHS / HG / HG-00249; United States / NIGMS NIH HHS / GM / GM-32842; United States / NHGRI NIH HHS / HG / R01 HG000249
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Plant Proteins; 0 / Pyridines; 00QT8FX306 / 3-acetylpyridine; 0U46U6E8UK / NAD; 25X51I8RD4 / Niacinamide; 30KYC7MIAI / Aspartic Acid; EC 2.7.7.1 / Nicotinamide-Nucleotide Adenylyltransferase
  • [Other-IDs] NLM/ PMC2936527
  •  go-up   go-down


7. Shi F, Li Y, Li Y, Wang X: Molecular properties, functions, and potential applications of NAD kinases. Acta Biochim Biophys Sin (Shanghai); 2009 May;41(5):352-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular properties, functions, and potential applications of NAD kinases.
  • NAD kinase catalyzes the phosphorylation of NAD(H) to form NADP(H), using ATP as phosphoryl donor.
  • It is the only key enzyme leading to the de novo NADP(+)/NADPH biosynthesis.
  • Coenzymes such as NAD(H) and NADP(H) are known for their important functions.
  • Recent studies have partially demonstrated that NAD kinase plays a crucial role in the regulation of NAD(H)/NADP(H) conversion.
  • Here, the molecular properties, physiologic functions, and potential applications of NAD kinase are discussed.
  • [MeSH-major] Bacterial Proteins / metabolism. NAD / metabolism. NADP / metabolism. Phosphotransferases (Alcohol Group Acceptor) / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19430699.001).
  • [ISSN] 1745-7270
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Bacterial Proteins; 0U46U6E8UK / NAD; 53-59-8 / NADP; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.23 / NAD kinase
  • [Number-of-references] 73
  •  go-up   go-down


8. Smit NP, van Nieuwpoort FA, Marrot L, Out C, Poorthuis B, van Pelt H, Meunier JR, Pavel S: Increased melanogenesis is a risk factor for oxidative DNA damage--study on cultured melanocytes and atypical nevus cells. Photochem Photobiol; 2008 May-Jun;84(3):550-5
Genetic Alliance. consumer health - Nevus.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased melanogenesis is a risk factor for oxidative DNA damage--study on cultured melanocytes and atypical nevus cells.
  • We show that tyrosine-induced melanogenesis in cultured normal human melanocytes (NHM) is accompanied by increased production of ROS and decreased concentration of intracellular glutathione.
  • Clinical atypical (dysplastic) nevi (DN) regularly contain more melanin than do normal melanocytes (MC).
  • We also show that in these cultured DN cells three out of four exhibit elevated synthesis of pheomelanin and this is accompanied by their early senescence.
  • By using various redox-sensitive molecular probes, we demonstrate that cultured DN cells produce significantly more ROS than do normal MC from the same donor.
  • Our experiments employing single-cell gel electrophoresis (comet assay) usually reveal higher fragmentation of DNA in DN cells than in normal MC.
  • Even if in some cases the normal alkaline comet assay shows no differences in DNA fragmentation between DN cells and normal MC, the use of the comet assay with formamidopyrimidine DNA glycosylase can disclose that the DNA of the cultured DN cells harbor more oxidative damage than the DNA of normal MC from the same person.
  • [MeSH-major] DNA Damage. Dysplastic Nevus Syndrome / pathology. Melanins / biosynthesis. Melanocytes / radiation effects. Reactive Oxygen Species / metabolism. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Cells, Cultured. Humans. Oxidative Stress / radiation effects. Pigmentation. Risk Factors. Skin / cytology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18435613.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Melanins; 0 / Reactive Oxygen Species
  •  go-up   go-down


9. Pizzichetta MA, Massone C, Soyer HP: Regression of atypical nevus: an anecdotal dermoscopic observation. Dermatol Surg; 2006 Oct;32(10):1274-7
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of atypical nevus: an anecdotal dermoscopic observation.
  • BACKGROUND: Clark nevi (atypical melanocytic nevi) can be considered as risk markers and potential precursors of melanoma.
  • The authors report on the morphologic changes of an atypical nevus by dermoscopic follow-up examination over a 7-year period.
  • After 7 months, the area of peripheral eccentric hyperpigmentation had regressed, and after 4.5 years the atypical pigment network had almost disappeared.
  • After 7 years of follow-up, a diffuse area of hypopigmentation and a residual light brown pigmentation were detectable.
  • The histopathologic diagnosis was consistent with an atypical junctional nevus with regression with features of a Clark nevus.
  • CONCLUSION: Based on our observation, even a dermoscopically atypical nevus may undergo regression as documented by long-term dermoscopic follow-up.
  • [MeSH-major] Dermoscopy. Neoplasm Regression, Spontaneous / pathology. Nevus / pathology. Skin Neoplasms / pathology

  • Genetic Alliance. consumer health - Nevus.
  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17034379.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


10. de Snoo FA, Kroon MW, Bergman W, ter Huurne JA, Houwing-Duistermaat JJ, van Mourik L, Snels DG, Breuning MH, Willemze R, Frants RR, Gruis NA: From sporadic atypical nevi to familial melanoma: risk analysis for melanoma in sporadic atypical nevus patients. J Am Acad Dermatol; 2007 May;56(5):748-52
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] From sporadic atypical nevi to familial melanoma: risk analysis for melanoma in sporadic atypical nevus patients.
  • BACKGROUND: Atypical nevi (AN), present in either a familial or a sporadic setting, are strong indicators of increased melanoma risk.
  • Six of 167 patients were carriers of a CDKN2A mutation.
  • At the end of follow-up, 10 of 136 patients with sporadic AN reported being a member of a melanoma family.
  • LIMITATIONS: This study was conducted in an area with a founder mutation in many of its melanoma families; therefore the results may not be applicable to other populations.
  • [MeSH-major] Dysplastic Nevus Syndrome / genetics. Melanoma / genetics. Skin Neoplasms / genetics

  • Genetic Alliance. consumer health - Melanoma, familial.
  • Genetic Alliance. consumer health - Nevus.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17276542.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


11. Lorentzen HF, Weismann K: [Dynamic dermoscopy]. Ugeskr Laeger; 2006 Nov 20;168(47):4105-6
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In patients with atypical nevus syndrome or more than 50 nevi, repetitive excision of benign lesions does not guarantee that melanomas will be identified at an early stage and exposes patients to potentially disfiguring surgery.
  • We present the case of a high-risk patient where repeated dermoscopy of an in situ melanoma showed that part of the pigment network had coarsened, even though the lesion had not changed macroscopically.
  • [MeSH-major] Carcinoma in Situ / pathology. Dermoscopy. Melanoma / pathology. Nevus / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Male. Nevus, Pigmented / pathology

  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17134611.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Denmark
  •  go-up   go-down


12. Wolf O, Shalom A: [Dermoscopy--a glimpse into the skin]. Harefuah; 2010 Aug;149(8):519-23, 550
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Dermoscopy--a glimpse into the skin].
  • The acronym ABCDE, which was originally described to help with clinically discriminating between benign and malignant pigmented skin lesions, represents the key clinical criteria for diagnosing cutaneous malignant melanoma (CMM).
  • The early stage in CMM is sometimes hard to identify for it frequently mimics the characteristics of atypical nevus.
  • It is estimated that clinical diagnosis accuracy in CMM lies somewhere between 50-75%.
  • During the last decade, and specifically with the advances in dermoscopy, also known as dermatoscopy or epiluminescence microscopy (ELM), there is literally a new depth and dimension to the clinical diagnosis of pigmented skin lesions.
  • What strikes out as its distinct clinical advantage is its ability to differentiate between an atypical nevus--for which follow-up is the preferred clinical choice, and CMM--which warrants surgical treatment at an early stage.
  • This edge dermoscopy process, put together with a digital interface applied in total-body mapping--as practiced in directed centers, may help decrease the number of false positive excisions without an increase in morbidity from CMM.
  • [MeSH-major] Dermoscopy / methods. Melanoma / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] False Positive Reactions. Humans. Nevus / diagnosis. Nevus / pathology

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21341432.001).
  • [ISSN] 0017-7768
  • [Journal-full-title] Harefuah
  • [ISO-abbreviation] Harefuah
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Israel
  •  go-up   go-down


13. Campos-do-Carmo G, Ramos-e-Silva M: Dermoscopy: basic concepts. Int J Dermatol; 2008 Jul;47(7):712-9
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dermoscopy is a very useful technique for the analysis of pigmented skin lesions.
  • It represents a link between clinical and histological views, permitting an earlier diagnosis of skin melanoma.
  • It also helps in the diagnosis of many other pigmented skin lesions, such as seborrheic keratosis, pigmented basal cell carcinoma, hemangioma, blue nevus, atypical nevus, and mole, which can often clinically simulate melanoma.
  • [MeSH-major] Dermatology / instrumentation. Dermoscopy / methods. Melanoma / diagnosis. Nevus, Pigmented / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Dysplastic Nevus Syndrome / diagnosis. Dysplastic Nevus Syndrome / pathology. Equipment Design. Equipment Safety. Humans. Precancerous Conditions / diagnosis. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18613881.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 22
  •  go-up   go-down


14. Kolman O, Hoang MP, Piris A, Mihm MC Jr, Duncan LM: Histologic processing and reporting of cutaneous pigmented lesions: recommendations based on a survey of 94 dermatopathologists. J Am Acad Dermatol; 2010 Oct;63(4):661-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • (2) determine the impact of the procedure, intent to excise, and histologic diagnosis on the process of margin evaluation; and (3) propose guidelines based on these findings.
  • METHODS: The survey consisted of 44 questions focused on the impact of procedure (punch, shave, or ellipse), intent (excision or biopsy), and histologic diagnosis (common nevus, congenital nevus, atypical nevus, melanoma) on processing and margin reporting.
  • Although more than 90% of observers report the margins on all melanomas and atypical nevi, fewer than 50% of respondents report margins on all nonatypical nevi.
  • LIMITATIONS: The study consists of a survey sample of dermatopathologists and does not represent the practices of those who did not respond to the survey.
  • (3) obtain levels in cases with tumor in the tip but not at ink if the specimen is an ellipse or excision and the diagnosis is atypical nevus or melanoma; and (4) report margins on all atypical nevi and melanomas.
  • [MeSH-major] Dermatology / methods. Dermatology / statistics & numerical data. Dysplastic Nevus Syndrome / pathology. Melanoma / pathology. Pathology, Surgical / methods. Practice Patterns, Physicians' / statistics & numerical data. Skin Neoplasms / pathology
  • [MeSH-minor] Academic Medical Centers. Attitude of Health Personnel. Biopsy, Needle. Diagnosis, Differential. Female. Health Care Surveys. Humans. Immunohistochemistry. Male. Massachusetts. Practice Guidelines as Topic. Risk Assessment. Surveys and Questionnaires

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2009 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20846568.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Kmetz EC, Sanders H, Fisher G, Lang PG, Maize JC Sr: The role of observation in the management of atypical nevi. South Med J; 2009 Jan;102(1):45-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of observation in the management of atypical nevi.
  • OBJECTIVE: The definition and management of the atypical nevus remains a controversial issue.
  • Some believe that atypical nevi are common variants of benign melanocytic nevi while others believe they are lesions intermediate between benign melanocytic nevi and melanoma.
  • Therefore, the question of whether or not partially removed atypical nevi should be re-excised with clear margins in order to prevent their evolution into melanoma remains unanswered.
  • Although studies have shown that most atypical nevi will never progress into melanoma, re-excision, when biopsy margins are positive, is commonly practiced.
  • METHODS: Our cohort study includes 55 previously biopsied atypical nevi that were not re-excised and which were followed for at least 5 years with a mean follow up time of 6.12 years.
  • RESULTS: The experimental group included 26 atypical nevi whose biopsy revealed at least one involved margin.
  • The control group included 29 atypical nevi whose biopsy revealed clear margins.
  • No melanomas were observed to arise in association with a pre-existing atypical nevus in either the experimental or control group during the follow-up period.
  • CONCLUSIONS: The results of our study support observation as a safe alternative to re-excision for incompletely removed atypical nevi.
  • A large prospective study with longer follow up would be necessary to better answer the question of how often atypical nevi evolve into melanoma and over what time period this occurs.
  • [MeSH-major] Dysplastic Nevus Syndrome / surgery. Neoplasm Recurrence, Local / prevention & control. Observation. Skin Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19077745.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Pishvaian MJ, Marshall JL, Hwang JJ, Malik S, He AR, Deeken JF, Kelso CB, Cotarla I, Berger MS: A phase I trial of GMX1777, an inhibitor of nicotinamide phosphoribosyl transferase (NAMPRT), given as a 24-hour infusion. J Clin Oncol; 2009 May 20;27(15_suppl):3581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of GMX1777, an inhibitor of nicotinamide phosphoribosyl transferase (NAMPRT), given as a 24-hour infusion.
  • : 3581 Background: GMX1777 is a pro-drug which converts to GMX1778, a potent and specific small molecule inhibitor of NAMPRT, the rate-limiting enzyme in NAD+ synthesis.
  • Thrombocytopenia, GI hemorrhage, and skin rash (the last occurring after multiple cycles) were encountered at higher doses.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961760.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Mazzone PJ, Videtic G, Murthy S, Mason D, Rice T, Pennell N, Rich T, Machuzak M, Mekhail T: The serial effects of multimodality therapy for stage III non-small cell carcinoma on lung function. J Clin Oncol; 2009 May 20;27(15_suppl):7551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7551 Purpose: To describe the effects of multimodality treatment on lung function in patients with stage III non-small cell carcinoma of the lung (NSCLC) Methods: Pulmonary function tests (PFTs) were reviewed for 32 patients with stage III NSCLC who were enrolled in a multimodality protocol that included neoadjuvant (NAd) combined chemoradiotherapy (taxol 50 mg/m2, carboplatin AUC 2 weekly X 3, radiation (XRT) 1.8 Gy BID to 30 Gy + erlotinib 150 mg/d for 28 days, followed by resection (R) and adjuvant (Ad) chemoradiotherapy (same as induction) followed by erlotinib 150mg/d maintenance (M) for 2 years.
  • Changes in PFTs were analyzed at multiple time points (baseline to after NAd, after NAd to after R, after R to after Ad) and for the overall effect of treatment (baseline to the end of treatment).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963339.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Hensel M, Goetzenich A, Hanhoff N, Wolf E, Knechten H, Mosthaf F: Cancer incidence in HIV-positive patients in Germany: A nation-wide survey from 2000 to 2007. J Clin Oncol; 2009 May 20;27(15_suppl):e22115

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of this study was to gather data on the epidemiology of AIDS-defining (AD) and non-AIDS-defining (NAD) malignancies in HIV-positive patients (pts) in Germany in the past decade.
  • Among the 299 cases (54.2%) of NAD malignomas were 213 solid tumors including 71 anal carcinomas (= 33.5% of all NAD malignancies) and 85 hemoblastoses including 29 Hodgkin lymphomas (= 9.6% of all NAD malignancies).
  • The high proportion of NAD malignancies has remained constant over all observation periods, as well as the relative incidence of most of the different subentities.
  • CONCLUSIONS: Our observations show a high incidence of NAD malignomas over the past 8 years in Germany.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963512.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Frankenthaler A, Lee M, Seery V, Renzi S, Kinnaman M, Liu V, Friedman E, Atkins MB, Cutaneous Oncology Program: Impact of concomitant immunosuppression on the presentation and prognosis of patients with melanoma. J Clin Oncol; 2009 May 20;27(15_suppl):9070

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We examined the Beth Israel Deaconess Medical Center Cutaneous Oncology Program database for pts with immune suppression at the time of melanoma diagnosis.
  • Melanoma stages at diagnosis were in situ 1, IB 7, IIA 1, IIB 1, IIIB 3, IIIC 5, and IV 1.
  • In addition, more cases appeared to have an amelanotic primary (21% vs. 5.4%) or an atypical mole syndrome (21% vs 10.2%).
  • At a median f/up of 52 mos, 37% of the cases had relapsed and all of these pts had died.
  • At a median f/up of 76 mos, 30% of the controls had relapsed yet only 47% of these pts had died.
  • CONCLUSIONS: Compared to the general melanoma population, pts with concomitant immune suppression appear more likely to be female, have an amelanotic primary or atypical mole syndrome and more advanced disease at presentation.
  • Thus, diagnosis and treatment of a primary melanoma at an early stage appears especially important in an immunosuppressed population.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962173.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Palicka GA, Rhodes AR: Acral melanocytic nevi: prevalence and distribution of gross morphologic features in white and black adults. Arch Dermatol; 2010 Oct;146(10):1085-94
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acral melanocytic nevi: prevalence and distribution of gross morphologic features in white and black adults.
  • OBJECTIVE: To determine prevalence and morphologic features of acral melanocytic nevi in white and black adults.
  • MAIN OUTCOME MEASURES: Prevalence and morphologic features based on ethnicity, sex, and age.
  • RESULTS: Palmar or plantar nevi were detected in 42.0% of blacks (50 of 119) vs 23.0% of whites (79 of 343) (P < .001).
  • Palmar or plantar nevi of 6-mm diameter or larger were detected in 3.4% of blacks (4 of 119) vs 0.6% of whites (2 of 343) (P = .04).
  • Diffusely black acral nevi were uncommon in whites (0 of 343) and blacks (1 of 119).
  • The prevalence of palmar or plantar nevi increased directly with degree of skin pigmentation (P < .001).
  • In whites, this prevalence was greater in women (27.1%, 51 of 188) than in men (18.1%, 28 of 155) (P = .047); in subjects younger than 50 years (30.8%, 57 of 185) than in those 50 years or older (13.9%, 22 of 158) (P < .001); in subjects with a history of atypical nevus removal than in those without (odds ratio [OR], 3.6; 95% confidence interval [CI], 1.9-6.9); in those with at least 1 extant atypical nevus than in those without (OR, 3.2; 95% CI, 1.7-6.0); and in those with at least 20 nevi of 2-mm diameter or larger than in those without (OR, 3.0; 95% CI, 1.6-5.6).
  • CONCLUSIONS: Acral nevi appear to be associated with ethnicity, pigmentation, age, and cutaneous melanoma (CM) risk factors.
  • While relatively large and/or very darkly pigmented acral nevi appear to be more common in blacks than in whites, diffusely black acral nevi are uncommon in both groups.
  • These findings are relevant to the assessment of pigmented lesions in the differential diagnosis of acral CM.
  • [MeSH-major] African Americans. European Continental Ancestry Group. Nevus, Pigmented / epidemiology. Nevus, Pigmented / pathology. Skin Neoplasms / epidemiology. Skin Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - African American Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20956637.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


21. Seidenari S, Pellacani G, Martella A: Acquired melanocytic lesions and the decision to excise: role of color variegation and distribution as assessed by dermoscopy. Dermatol Surg; 2005 Feb;31(2):184-9
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Because melanoma may sometimes be difficult to differentiate from nevi with clinical atypia, many benign lesions also undergo surgical removal.
  • METHODS: Overall, 603 images, referring to 112 melanomas and 491 nevi, were retrospectively subdivided into four groups: "clearly benign," "follow-up," "dermoscopic atypical nevi," and "dermoscopic melanomas," according to their dermoscopic aspects.
  • RESULTS: With respect to lesions not eligible for excision according to dermoscopy (but excised for cosmetic reasons), those excised with a suspicion of malignancy showed a higher number of colors, whose distribution was also more asymmetric.
  • Moreover, the frequency of the presence of black and blue-gray progressively increased from clearly benign lesions to atypical nevi and dermoscopic melanomas.
  • CONCLUSION: In dermoscopic images, color parameters are essential elements for the diagnosis of atypical nevus, which can be differentiated from both a clearly benign lesion and a melanoma.
  • [MeSH-major] Melanoma / diagnosis. Melanoma / surgery. Microscopy / methods. Skin Neoplasms / diagnosis. Skin Neoplasms / surgery
  • [MeSH-minor] Decision Support Techniques. Humans. Nevus, Pigmented / diagnosis. Nevus, Pigmented / pathology. Nevus, Pigmented / surgery. Predictive Value of Tests. ROC Curve. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15762212.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


22. Uribe P, Wistuba II, Gonzalez S: Allelotyping, microsatellite instability, and BRAF mutation analyses in common and atypical melanocytic nevi and primary cutaneous melanomas. Am J Dermatopathol; 2009 Jun;31(4):354-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allelotyping, microsatellite instability, and BRAF mutation analyses in common and atypical melanocytic nevi and primary cutaneous melanomas.
  • Loss of heterozygosity (LOH) in several chromosomal regions is found in melanoma, and it has been partially studied in nevi.
  • BRAF mutations are found in melanoma and nevi and in colorectal cancer are linked to mismatch repair deficiency.
  • DNA extracted from microdissected cells of 22 common nevi, 23 atypical nevi, and 25 primary cutaneous melanomas were examined for LOH and MSI by polymerase chain reaction-based analysis of 24 microsatellite markers and BRAF mutation.
  • Allelic loss index was higher in atypical nevi (0.20) and melanomas (0.27) than common nevi (0.07).
  • LOH at any of this loci occurred in 27% of common nevi, 57% of atypical nevi, and 68% of melanomas.
  • Similar genetic alterations in atypical nevi and melanomas support the concept of atypical nevus as melanoma precursor.
  • Novel deletion loci at 5q35 and 17q21 (BRCA1) in atypical nevi and melanomas were identified.
  • [MeSH-major] Loss of Heterozygosity. Microsatellite Instability. Nevus, Pigmented / genetics. Proto-Oncogene Proteins B-raf / genetics. Skin Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19461239.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  •  go-up   go-down


23. Fernandes JD, Machado MC, Oliveira ZN: Increased melanocytic nevi in patients with inherited ichthyoses: report of a previously undescribed association. Pediatr Dermatol; 2010 Sep-Oct;27(5):453-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased melanocytic nevi in patients with inherited ichthyoses: report of a previously undescribed association.
  • Ichthyosis is a heterogeneous cornification disorder.
  • The objective of this study was to evaluate the clinical, dermoscopic, and histopathologic features of nevi and lentigines in 16 patients with autosomal recessive congenital ichthyosis-lamellar ichthyosis and nonbullous ichthyosiform congenital erythroderma.
  • Most patients (n = 13) reported no personal or familial history of melanoma or atypical nevi.
  • All of the patients had at least five atypical melanocytic lesions.
  • Ten of the 16 patients had at least one atypical nevus or lentigo.
  • This study suggests that increased atypical melanocytic nevi may be a feature of long-standing congenital ichthyoses.
  • As an unequivocal discrimination from malignant melanoma in vivo is not always possible, regular clinical follow-up of patients with ichthyosis and increased or unusual nevi is recommended.
  • [MeSH-major] Ichthyosis / epidemiology. Ichthyosis / pathology. Nevus, Pigmented / epidemiology. Nevus, Pigmented / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 20561241.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


24. Zangari A, Bernardini ML, Tallarico R, Ilari M, Giangiacomi M, Offidani AM, Martino A: Indications for excision of nevi and melanoma diagnosed in a pediatric surgical unit. J Pediatr Surg; 2007 Aug;42(8):1412-6
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Indications for excision of nevi and melanoma diagnosed in a pediatric surgical unit.
  • Its management relies on early diagnosis.
  • The purpose of this study is to discuss surgical indications of nevi and diagnosis of melanoma in a pediatric surgical unit.
  • METHODS: Data relative to the patients who underwent removal of nevi in our pediatric surgical unit from 1999 to 2005 were reviewed to identify indications, histology, and melanoma occurrence.
  • RESULTS: The most frequent indication was atypical nevus.
  • Compound nevus was the most common finding, followed by congenital and Spitz nevi.
  • Melanoma was diagnosed in 3 excised nevi, and in 1 case it occurred as a metastatic disease.
  • CONCLUSIONS: Our data showed a pattern of indications for surgery similar to that described in the literature, with a high detection rate of melanoma, nonetheless showing that some rare conditions may delay diagnosis.
  • [MeSH-major] Melanoma / diagnosis. Nevus / diagnosis. Skin Neoplasms / diagnosis. Skin Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17706506.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


25. Wang SQ, Dusza SW, Scope A, Braun RP, Kopf AW, Marghoob AA: Differences in dermoscopic images from nonpolarized dermoscope and polarized dermoscope influence the diagnostic accuracy and confidence level: a pilot study. Dermatol Surg; 2008 Oct;34(10):1389-95
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The objective was to evaluate whether diagnosis and diagnostic confidence changes when viewing dermoscopic images from NPDs and PDs.
  • Twenty-five pigmented lesions were shown in the study, consisting of 7 seborrheic keratoses (SK), 3 basal cell carcinomas, 2 atypical nevi, 5 malignant melanomas (MM), 3 dermatofibromas, 3 blue nevi, and 2 hemangiomas.
  • Significant differences in the diagnoses were observed for the SK, atypical nevus, and MM images.
  • CONCLUSIONS: Viewing lesions with NPD versus PD can affect the diagnosis and diagnostic confidence of physicians that are novices with dermoscopy.
  • Further studies including physicians at different expertise levels and a larger sample of lesions are needed to further explore the differences.
  • [MeSH-major] Dermoscopy / instrumentation. Skin Diseases / diagnosis
  • [MeSH-minor] Humans. Microscopy, Polarization. Pigmentation Disorders / diagnosis. Pilot Projects. Skin Neoplasms / diagnosis


26. McHugh JB, Fullen DR: Atypical compound nevus arising in mature cystic ovarian teratoma. Med Sci Monit; 2006 Apr;12(4):CS34-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical compound nevus arising in mature cystic ovarian teratoma.
  • Melanocytic nevi have also rarely been reported in MCOT.
  • CASE REPORT: A 28 year-old female presented with a palpable, 4.6 cm, right pelvic mass on physical examination.
  • A 2.0 x 1.0 cm pigmented area corresponded to a nevus with architectural and cytologic features of the so-called "dysplastic nevus," including variable-sized nests of nevomelanocytes irregularly distributed on distorted rete ridges, bridging of nests between rete ridges, fibroplasia around rete ridges, and junctional shouldering beyond the dermal nevus.
  • The nevomelanocytes demonstrated moderate cytologic atypia.
  • CONCLUSIONS: Herein, we report, to the best of our knowledge, the first case of an atypical ("dysplastic") nevus, arising in a MCOT.
  • Rarely, melanocytic nevi and melanomas arise from the ectodermal component of MCOTs.
  • Moreover, melanomas may arise de novo or in association with a nevus.
  • Distinction between a melanocytic nevus, as in our case, and a primary melanoma is critical for determining the patient's prognosis and need for additional therapy.
  • As primary ovarian melanomas, like their skin counterpart, may arise from a precursor lesion, removal of a melanocytic nevus, such as this atypical nevus, could theoretically prevent melanoma transformation.
  • [MeSH-major] Neoplasms, Multiple Primary / diagnosis. Nevus, Pigmented / diagnosis. Ovarian Neoplasms / diagnosis. Teratoma / diagnosis

  • Genetic Alliance. consumer health - Nevus.
  • Genetic Alliance. consumer health - Teratoma.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16572057.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


27. Nagore E, Botella-Estrada R, Garcia-Casado Z, Requena C, Serra-Guillen C, Llombart B, Sanmartin O, Guillen C: Comparison between familial and sporadic cutaneous melanoma in Valencia, Spain. J Eur Acad Dermatol Venereol; 2008 Aug;22(8):931-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Some clinical, pathological and genetic features have been associated to familial melanoma, particularly multiple melanoma and earlier age at diagnosis.
  • To compare the clinical, epidemiological and pathological differences between familial and sporadic melanoma patients in Valencia, Spain, a series of 959 patients with cutaneous melanoma were selected at a single institution.
  • For this study the following variables were selected: age, sex, melanoma site and presence of solar lentigines on the melanoma surrounding skin, histological subtype, tumor thickness, stage, family and personal history of cutaneous melanoma and of other neoplasias, personal history of non-melanoma skin cancer, past personal history of severe sunburns, cutaneous phenotype (phototype, hair and eyes colors number of common nevus, number of atypical nevi, presence of solar lentigines).
  • Among the multiple variables studied, a younger age at diagnosis (median age of 42 vs 53 years), higher frequency of the presence of at least one clinically atypical nevus (36.1% vs 17.7%), multiple melanomas (12.2% vs 3.4%) and red/blonde hair (33.3% vs 18.9%), and a lower rate of cases with solar lentigines in melanoma site (33.3% vs 56.3%) were found for familial cases.
  • In summary, phenotypic risk factors for familial melanoma are a tendency to develop multiple melanomas, to have clinically atypical nevi and to present less actinic damage at the melanoma site.
  • All these results enhance the relevancy of genetic susceptibility associated to the ability to produce atypical nevi and partly to a higher sensitivity to the sun.
  • [MeSH-major] Melanoma / genetics. Melanoma / pathology. Skin Neoplasms / genetics. Skin Neoplasms / pathology

  • Genetic Alliance. consumer health - Melanoma, familial.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18355200.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


28. Waller JM, Zedek DC: How informative are dermatopathology requisition forms completed by dermatologists? A review of the clinical information provided for 100 consecutive melanocytic lesions. J Am Acad Dermatol; 2010 Feb;62(2):257-61
MedlinePlus Health Information. consumer health - Skin Conditions.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Accurate clinicopathologic correlation can be crucial to arriving at the correct microscopic diagnosis.
  • Dermatoscopy information and a clinical photograph were provided once each.
  • In 19 cases, the only information on the requisition form was one of the phrases: "r/o atypia," "r/o atypical nevus," "r/o Clark's," or "r/o dysplastic nevus."
  • In 10 cases, the only information was "r/o nevus."
  • [MeSH-major] Dermatology. Medical Records / standards. Melanoma / pathology. Referral and Consultation / standards. Skin Diseases / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Biopsy. Humans. Pathology, Clinical. Skin / pathology

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
  • (PMID = 19962786.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


29. Carli P, Ghigliotti G, Gnone M, Chiarugi A, Crocetti E, Astorino S, Berti UA, Broganelli P, Carcaterra A, Corradin MT, Pellacani G, Piccolo D, Risulo M, Stanganelli I, De Giorgi V: Baseline factors influencing decisions on digital follow-up of melanocytic lesions in daily practice: an Italian multicenter survey. J Am Acad Dermatol; 2006 Aug;55(2):256-62
International Agency for Research on Cancer - Screening Group. diagnostics - Planning and Implementing Cervical Cancer Prevention and Control Programs: A Manual for Managers .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Predictors of a short follow-up interval (<or=3 months) compared with a 6-month interval were investigated by means of logistic regression analysis.
  • Determinants of a short follow-up interval, adopted in 40.8% of patients, were the personal history of melanoma (odds ratio [OR] 2.56, 95% confidence interval [CI] 1.09-5.99) and the presence of atypical nevi (at least one atypical nevus (OR 4.54, 95% CI 2.45-8.42).
  • Unexpectedly, the dermoscopic atypia of the lesion (TDS >4.75) was associated only with a marginal effect on the scheduled duration of follow-up interval (OR 1.34, 95% CI 0.97-1.86).
  • [MeSH-major] Image Processing, Computer-Assisted. Mass Screening / methods. Melanoma / diagnosis. Skin Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16844508.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study
  • [Publication-country] United States
  •  go-up   go-down


30. Niemiec P, Zak I: [Vascular NAD(P)H oxidases--role in the pathogenesis of atherosclerosis]. Postepy Biochem; 2005;51(1):1-11
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Vascular NAD(P)H oxidases--role in the pathogenesis of atherosclerosis].
  • [Transliterated title] Naczyniowe oksydazy NAD(P)H--znaczenie w patogenezie miazdzycy.
  • Vascular NAD(P)H oxidases are multicomponent enzymes found in vascular smooth muscle cells and endothelial cells.
  • Vascular NAD(P)H oxidases are predominant sources of superoxide in the vasculature.
  • Active forms of NAD(P)H oxidases are associated with plasma membrane and consist of at least six components, namely: NOX, p22phox peptides and p47phox, p67phox, p40phox and Rac.
  • Angiotensin II is the most important activator of NAD(P)H oxidases in vasculature.
  • Moreover, reactive oxygen species produced by NAD(P)H oxidases may be involved in endothelial cells apoptosis, oxidation of low density lipoproteins and vascular myocytes hypertrophy and proliferation.
  • Specific inhibitors of NAD(P)H oxidases may be useful experimental tools for atherosclerosis research and may have potential therapeutic significance in the future.

  • MedlinePlus Health Information. consumer health - Atherosclerosis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16209336.001).
  • [ISSN] 0032-5422
  • [Journal-full-title] Postepy biochemii
  • [ISO-abbreviation] Postepy Biochem.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 11062-77-4 / Superoxides; 11128-99-7 / Angiotensin II; EC 1.6.3.1 / NADPH Oxidase
  • [Number-of-references] 92
  •  go-up   go-down


31. Billington RA, Genazzani AA, Travelli C, Condorelli F: NAD depletion by FK866 induces autophagy. Autophagy; 2008 Apr;4(3):385-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD depletion by FK866 induces autophagy.
  • NAD is a multifunctional molecule involved in both metabolic processes and signaling pathways.
  • Such signalling pathways consume NAD which is replenished via one of several biosynthesis pathways.
  • We show that influx of NAD across the plasma membrane may be able to contribute to the homeostasis of intracellular NAD levels.
  • Indeed, extracellular application of NAD was able to replete NAD levels that had been lowered pharmacologically using the novel drug FK866 and was also able to rescue cells from FK866-induced cell death.
  • A marked lag between the drop in NAD levels and cell death prompted us to investigate the mechanism of cell death.
  • Furthermore, this autophagic phenotype could be reverted by the addition of NAD to the extracellular medium.
  • [MeSH-major] Acrylamides / pharmacology. Antineoplastic Agents / pharmacology. Autophagy / drug effects. NAD / physiology. Piperidines / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18227641.001).
  • [ISSN] 1554-8635
  • [Journal-full-title] Autophagy
  • [ISO-abbreviation] Autophagy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Antineoplastic Agents; 0 / Apoptosis Inducing Factor; 0 / Microtubule-Associated Proteins; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0 / light chain 3, human; 0U46U6E8UK / NAD; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


32. Billington RA, Travelli C, Ercolano E, Galli U, Roman CB, Grolla AA, Canonico PL, Condorelli F, Genazzani AA: Characterization of NAD uptake in mammalian cells. J Biol Chem; 2008 Mar 7;283(10):6367-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of NAD uptake in mammalian cells.
  • Recent evidence has shown that NAD(P) plays a variety of roles in cell-signaling processes.
  • Surprisingly, the presence of NAD(P) utilizing ectoenzymes suggests that NAD(P) is present extracellularly.
  • Indeed, nanomolar concentrations of NAD have been found in plasma and other body fluids.
  • Although very high concentrations of NAD have been shown to enter cells, it is not known whether lower, more physiological concentrations are able to be taken up.
  • Here we show that two mammalian cell types are able to transport low NAD concentrations effectively.
  • Furthermore, extracellular application of NAD was able to counteract FK866-induced cell death and restore intracellular NAD(P) levels.
  • We propose that NAD uptake may play a role in physiological NAD homeostasis.
  • [MeSH-major] NAD / metabolism. NADP / metabolism. Signal Transduction / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18180302.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; 53-59-8 / NADP
  •  go-up   go-down


33. Gazzaniga F, Stebbins R, Chang SZ, McPeek MA, Brenner C: Microbial NAD metabolism: lessons from comparative genomics. Microbiol Mol Biol Rev; 2009 Sep;73(3):529-41, Table of Contents
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microbial NAD metabolism: lessons from comparative genomics.
  • NAD is a coenzyme for redox reactions and a substrate of NAD-consuming enzymes, including ADP-ribose transferases, Sir2-related protein lysine deacetylases, and bacterial DNA ligases.
  • Microorganisms that synthesize NAD from as few as one to as many as five of the six identified biosynthetic precursors have been identified.
  • De novo NAD synthesis from aspartate or tryptophan is neither universal nor strictly aerobic.
  • Salvage NAD synthesis from nicotinamide, nicotinic acid, nicotinamide riboside, and nicotinic acid riboside occurs via modules of different genes.
  • Nicotinamide salvage genes nadV and pncA, found in distinct bacteria, appear to have spread throughout the tree of life via horizontal gene transfer.
  • [MeSH-major] Bacteria. Genomics. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Bacteriol. 2001 Feb;183(4):1168-74 [11157928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3083-8 [19204287.001]
  • [Cites] Mol Microbiol. 2001 Jun;40(6):1241-8 [11442824.001]
  • [Cites] Science. 2001 Dec 14;294(5550):2310-4 [11743192.001]
  • [Cites] Structure. 2002 Jan;10(1):69-79 [11796112.001]
  • [Cites] J Biol Chem. 2002 Feb 1;277(5):3698-707 [11704676.001]
  • [Cites] Yeast. 2002 Feb;19(3):215-24 [11816029.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):497-502 [11823852.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18881-90 [11884393.001]
  • [Cites] J Biol Chem. 2002 Sep 6;277(36):33291-9 [12068016.001]
  • [Cites] Extremophiles. 2002 Aug;6(4):275-81 [12215812.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45099-107 [12297502.001]
  • [Cites] J Bacteriol. 2002 Dec;184(24):6906-17 [12446641.001]
  • [Cites] Cell. 2002 Nov 27;111(5):747-56 [12464185.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):15908-13 [12456892.001]
  • [Cites] J Biol Chem. 2003 Mar 7;278(10):8804-8 [12496312.001]
  • [Cites] Mol Microbiol. 2003 Apr;48(1):77-84 [12657046.001]
  • [Cites] Bioinformatics. 2003 Aug 12;19(12):1572-4 [12912839.001]
  • [Cites] J Bacteriol. 2003 Sep;185(17):5220-33 [12923095.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33049-55 [12771147.001]
  • [Cites] Chem Biol. 2003 Dec;10(12):1195-204 [14700627.001]
  • [Cites] Infect Immun. 2004 Feb;72(2):1143-6 [14742562.001]
  • [Cites] Trends Biochem Sci. 2004 Mar;29(3):111-8 [15003268.001]
  • [Cites] Science. 2004 Apr 2;304(5667):66-74 [15001713.001]
  • [Cites] J Bacteriol. 2004 May;186(9):2862-71 [15090528.001]
  • [Cites] Cell. 2004 May 14;117(4):495-502 [15137942.001]
  • [Cites] J Biol Chem. 1967 Feb 10;242(3):385-92 [4290215.001]
  • [Cites] J Exp Med. 1969 Jan 1;129(1):1-21 [4304436.001]
  • [Cites] J Bacteriol. 1994 Jun;176(11):3400-2 [8195100.001]
  • [Cites] Science. 1995 Jul 28;269(5223):496-512 [7542800.001]
  • [Cites] Nat Med. 1996 Jun;2(6):662-7 [8640557.001]
  • [Cites] Eur J Biochem. 1996 Jul 15;239(2):427-33 [8706750.001]
  • [Cites] J Bacteriol. 1998 Jun;180(12):3218-21 [9620974.001]
  • [Cites] Nature. 2000 Feb 17;403(6771):795-800 [10693811.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jul 5;273(2):793-8 [10873683.001]
  • [Cites] FEBS Lett. 1999 Feb 12;444(2-3):222-6 [10050763.001]
  • [Cites] FEBS Lett. 1999 Jul 16;455(1-2):13-7 [10428462.001]
  • [Cites] J Bacteriol. 1999 Sep;181(17):5509-11 [10464228.001]
  • [Cites] J Biol Chem. 1951 Apr;189(2):889-99 [14832305.001]
  • [Cites] J Biol Chem. 1958 Aug;233(2):488-92 [13563526.001]
  • [Cites] J Biol Chem. 1958 Aug;233(2):493-500 [13563527.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D34-8 [15608212.001]
  • [Cites] Nat Genet. 2005 Feb;37(2):153-9 [15640799.001]
  • [Cites] Science. 2005 May 6;308(5723):866-70 [15774723.001]
  • [Cites] Structure. 2005 Sep;13(9):1239-40 [16154080.001]
  • [Cites] Structure. 2005 Sep;13(9):1385-96 [16154095.001]
  • [Cites] Nucleic Acids Res. 2005;33(17):5691-702 [16214803.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36334-41 [16118205.001]
  • [Cites] Science. 2006 Mar 3;311(5765):1283-7 [16513982.001]
  • [Cites] J Bacteriol. 2006 Apr;188(8):3012-23 [16585762.001]
  • [Cites] Plant Physiol. 2006 Jul;141(3):851-7 [16698895.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D224-8 [17202162.001]
  • [Cites] Trends Biochem Sci. 2007 Jan;32(1):12-9 [17161604.001]
  • [Cites] Biochemistry. 2007 Apr 24;46(16):4912-22 [17402747.001]
  • [Cites] Cell. 2007 May 4;129(3):473-84 [17482543.001]
  • [Cites] Mol Microbiol. 2007 Oct;66(1):14-25 [17725566.001]
  • [Cites] PLoS Biol. 2007 Oct 2;5(10):e263 [17914902.001]
  • [Cites] Structure. 2008 Feb;16(2):196-209 [18275811.001]
  • [Cites] Nucleic Acids Res. 2008 Apr;36(6):2047-59 [18276643.001]
  • [Cites] Nucleic Acids Res. 2008 Apr;36(6):2032-46 [18276644.001]
  • [Cites] J Biol Chem. 2008 Jul 11;283(28):19329-41 [18490451.001]
  • [Cites] Annu Rev Nutr. 2008;28:115-30 [18429699.001]
  • [Cites] J Biol Chem. 2009 Jan 2;284(1):158-64 [19001417.001]
  • [Cites] Genome Biol. 2001;2(1):REVIEWS0001 [11380987.001]
  • (PMID = 19721089.001).
  • [ISSN] 1098-5557
  • [Journal-full-title] Microbiology and molecular biology reviews : MMBR
  • [ISO-abbreviation] Microbiol. Mol. Biol. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD
  • [Number-of-references] 69
  • [Other-IDs] NLM/ PMC2738131
  •  go-up   go-down


34. Ying W: NAD+ and NADH in neuronal death. J Neuroimmune Pharmacol; 2007 Sep;2(3):270-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+ and NADH in neuronal death.
  • Increasing evidence has suggested that NAD+ and NADH mediate not only energy metabolism and mitochondrial functions, but also calcium homeostasis, aging, and cell death.
  • This article is written to provide an overview about the information suggesting significant roles of NAD+ and NADH in neuronal death in certain neurological diseases.
  • Our latest studies have suggested that intranasal administration with NAD+ can profoundly decrease ischemic brain damage.
  • These observations suggest that NAD+ administration may be a novel therapeutic strategy for some neurological diseases.
  • [MeSH-major] NAD / physiology. Neurons / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18040861.001).
  • [ISSN] 1557-1904
  • [Journal-full-title] Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
  • [ISO-abbreviation] J Neuroimmune Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD
  • [Number-of-references] 50
  •  go-up   go-down


35. Ansari HR, Raghava GP: Identification of NAD interacting residues in proteins. BMC Bioinformatics; 2010;11:160
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of NAD interacting residues in proteins.
  • Nicotinamide adenine dinucleotide (NAD+ or NAD) is one of the most commonly used organic cofactors in living cells, which plays a critical role in cellular metabolism, storage and regulatory processes.
  • In the past, several NAD binding proteins (NADBP) have been reported in the literature, which are responsible for a wide-range of activities in the cell.
  • Attempts have been made to derive a rule for the binding of NAD+ to its target proteins.
  • Thus a sequence and non-similarity based method is needed to characterize the NAD binding sites to help in the annotation.
  • In this study attempts have been made to predict NAD binding proteins and their interacting residues (NIRs) from amino acid sequence using bioinformatics tools.
  • RESULTS: We extracted 1556 proteins chains from 555 NAD binding proteins whose structure is available in Protein Data Bank.
  • Then we removed all redundant protein chains and finally obtained 195 non-redundant NAD binding protein chains, where no two chains have more than 40% sequence identity.
  • In this study all models were developed and evaluated using five-fold cross validation technique on the above dataset of 195 NAD binding proteins.
  • Gly, Tyr, Thr, His) in NAD interaction, residues like Ala, Glu, Leu, Lys are not preferred.
  • A support vector machine (SVM) based method has been developed using various window lengths of amino acid sequence for predicting NAD interacting residues and obtained maximum Matthew's correlation coefficient (MCC) 0.47 with accuracy 74.13% at window length 17.
  • CONCLUSION: For the first time a sequence-based method has been developed for the prediction of NAD binding proteins and their interacting residues, in the absence of any prior structural information.
  • The present model will aid in the understanding of NAD+ dependent mechanisms of action in the cell.
  • [MeSH-major] NAD / chemistry. Proteins / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 2009 Jan;37(Database issue):D195-200 [18842629.001]
  • [Cites] Protein Sci. 2003 May;12(5):923-9 [12717015.001]
  • [Cites] Bioinformatics. 2009 May 1;25(9):1192-4 [19251774.001]
  • [Cites] BMC Bioinformatics. 2009;10:105 [19358699.001]
  • [Cites] BMC Bioinformatics. 2008;9:312 [18637174.001]
  • [Cites] Curr Opin Struct Biol. 2003 Jun;13(3):389-95 [12831892.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D129-33 [14681376.001]
  • [Cites] Proteins. 2004 Apr 1;55(1):83-90 [14997542.001]
  • [Cites] Nature. 1976 Aug 19;262(5570):726 [183143.001]
  • [Cites] FASEB J. 1996 Sep;10(11):1257-69 [8836039.001]
  • [Cites] Mol Microbiol. 1996 Aug;21(4):667-74 [8878030.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Bioinformatics. 1999 Apr;15(4):327-32 [10320401.001]
  • [Cites] J Cell Biol. 2005 Aug 1;170(3):349-55 [16043516.001]
  • [Cites] Science. 2005 Aug 12;309(5737):1093-6 [16099990.001]
  • [Cites] Proteins. 2005 Nov 1;61(2):318-24 [16106377.001]
  • [Cites] Protein Eng Des Sel. 2006 Feb;19(2):67-75 [16403825.001]
  • [Cites] Bioinformatics. 2006 Jul 1;22(13):1658-9 [16731699.001]
  • [Cites] Curr Protein Pept Sci. 2006 Oct;7(5):395-406 [17073692.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D515-20 [17082206.001]
  • [Cites] Protein Pept Lett. 2007;14(6):575-80 [17627599.001]
  • [Cites] BMC Bioinformatics. 2007;8:337 [17854501.001]
  • [Cites] Nucleic Acids Res. 2008 Jan;36(Database issue):D618-22 [17720712.001]
  • [Cites] Proteins. 2008 Apr;71(1):189-94 [17932917.001]
  • [Cites] J R Soc Interface. 2009 Feb 6;6(31):129-47 [19019817.001]
  • (PMID = 20353553.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins; 0U46U6E8UK / NAD
  • [Other-IDs] NLM/ PMC2853471
  •  go-up   go-down


36. Huang X, El-Sayed IH, Yi X, El-Sayed MA: Gold nanoparticles: catalyst for the oxidation of NADH to NAD(+). J Photochem Photobiol B; 2005 Nov 1;81(2):76-83
Hazardous Substances Data Bank. GOLD, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gold nanoparticles: catalyst for the oxidation of NADH to NAD(+).
  • Nicotinamide adenine dinucleotide is an important coenzyme involved in the production of ATP, the fuel of energy, in every cell.
  • It alternates between the oxidized form NAD(+) and the reduced form dihydronicotinamide adenine dinucleotide (NADH) and serves as a hydrogen and electron carrier in the cellular respiratory processes.
  • In the present work, the catalytic effect of gold nanoparticles on the oxidization of NADH to NAD(+) was investigated.
  • The intensity of the 340 nm absorption band of NADH was found to decrease while that of the 260 nm band of NAD(+) was found to increase as the concentration of gold nanoparticles increased.
  • This gives a strong support that the conversion of NADH to NAD(+) is occurring on the surface of the gold nanoparticles, i.e.
  • [MeSH-major] Gold / chemistry. NAD / chemistry

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16125965.001).
  • [ISSN] 1011-1344
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 7440-57-5 / Gold
  •  go-up   go-down


37. Brenner C: Evolution of NAD biosynthetic enzymes. Structure; 2005 Sep;13(9):1239-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolution of NAD biosynthetic enzymes.
  • Two research groups have solved crystal structures of nicotinic acid phosphoribosyltransferase (PRTase) and made the argument that PRTases in three distinct pathways of nicotinamide adenine dinucleotide (NAD) biosynthesis evolved from a common ancestor (Shin et al., 2005 and Chappie et al., 2005).
  • [MeSH-major] Evolution, Molecular. NAD / biosynthesis. Pentosyltransferases / chemistry. Pentosyltransferases / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Structure. 2005 Sep;13(9):1385-96 [16154095.001]
  • [CommentOn] J Biol Chem. 2005 May 6;280(18):18326-35 [15753098.001]
  • (PMID = 16154080.001).
  • [ISSN] 0969-2126
  • [Journal-full-title] Structure (London, England : 1993)
  • [ISO-abbreviation] Structure
  • [Language] eng
  • [Publication-type] Comment; News
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; EC 2.4.2.- / Pentosyltransferases; EC 6.3.4.21 / nicotinate phosphoribosyltransferase
  •  go-up   go-down


38. Chen YG, Kowtoniuk WE, Agarwal I, Shen Y, Liu DR: LC/MS analysis of cellular RNA reveals NAD-linked RNA. Nat Chem Biol; 2009 Dec;5(12):879-81
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] LC/MS analysis of cellular RNA reveals NAD-linked RNA.
  • This technique revealed NAD-linked RNA in Escherichia coli and Streptomyces venezuelae.
  • Subsequent characterization showed that NAD is a 5' modification of RNA, cannot be installed in vitro through aberrant transcriptional initiation, is only found among smaller cellular RNAs and is present at a surprisingly high abundance of approximately 3,000 copies per cell.
  • [MeSH-major] Escherichia coli / chemistry. NAD / isolation & purification. RNA, Bacterial / isolation & purification. RNA, Fungal / isolation & purification. RNA, Transfer / isolation & purification. Streptomyces / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Mol Cell Biol. 2004 Jun;5(6):451-63 [15173824.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 May 12;106(19):7768-73 [19416889.001]
  • [Cites] Nature. 1975 Jan 31;253(5490):374-5 [163011.001]
  • [Cites] J Mol Evol. 1976 Mar 29;7(2):101-4 [1263263.001]
  • [Cites] J Mol Evol. 1978 Jun 20;11(2):163-8 [671563.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Jan;77(1):201-4 [6153795.001]
  • [Cites] J Bacteriol. 1984 Jun;158(3):769-76 [6373741.001]
  • [Cites] Methods Enzymol. 1990;193:796-824 [1706064.001]
  • [Cites] Nucleic Acids Res. 1994 Jun 25;22(12):2183-96 [7518580.001]
  • [Cites] J Mol Evol. 1995 Jun;40(6):551-8 [7643406.001]
  • [Cites] Proteins. 1998 Sep 1;32(4):414-24 [9726413.001]
  • [Cites] J Biol Chem. 1958 Mar;231(1):241-57 [13538965.001]
  • [Cites] Nature. 1950 Aug 5;166(4214):237-8 [15439258.001]
  • [Cites] Nucleic Acids Res. 2005;33(1):e2 [15640439.001]
  • [Cites] Nature. 2001 Jan 18;409(6818):387-90 [11201752.001]
  • [Cites] Annu Rev Biochem. 2001;70:39-80 [11395402.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 1;31(3):e8 [12560511.001]
  • [Cites] J Am Chem Soc. 2004 Apr 28;126(16):5044-5 [15099068.001]
  • [Cites] Mol Microbiol. 2005 Oct;58(2):456-66 [16194232.001]
  • [Cites] Mol Cell. 2007 Jul 6;27(1):79-90 [17612492.001]
  • [Cites] J Am Chem Soc. 2008 Nov 19;130(46):15611-26 [18956864.001]
  • [Cites] Biol Cell. 2009 Feb;101(2):117-31 [19076068.001]
  • [Cites] Cell. 2009 Feb 20;136(4):615-28 [19239884.001]
  • [Cites] Science. 2004 Sep 10;305(5690):1601-5 [15319493.001]
  • (PMID = 19820715.001).
  • [ISSN] 1552-4469
  • [Journal-full-title] Nature chemical biology
  • [ISO-abbreviation] Nat. Chem. Biol.
  • [Language] eng
  • [Databank-accession-numbers] PubChem-Substance/ 85195596/ 85195597/ 85195598/ 85195599
  • [Grant] United States / NIGMS NIH HHS / GM / R01GM065865; United States / NIGMS NIH HHS / GM / R01 GM065865-05A1; United States / Howard Hughes Medical Institute / / HHMI/ LIU/ D; United States / NIGMS NIH HHS / GM / R01 GM065865-06S1; United States / NIGMS NIH HHS / GM / R01 GM065865-06; United States / NIGMS NIH HHS / GM / R01 GM065865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Bacterial; 0 / RNA, Fungal; 0U46U6E8UK / NAD; 9014-25-9 / RNA, Transfer
  • [Other-IDs] NLM/ NIHMS140940; NLM/ PMC2842606
  •  go-up   go-down


39. Cvetić T, Veljović-Jovanović S, Vucinić Z: Characterization of NAD-dependent malate dehydrogenases from spinach leaves. Protoplasma; 2008;232(3-4):247-53
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of NAD-dependent malate dehydrogenases from spinach leaves.
  • Spinach leaves were used to extract isoforms of NAD-dependent malate dehydrogenase (NAD-MDH) (EC 1.1.1.37), either soluble or bound to microsomal, plasma, or chloroplast envelope membranes.
  • All fractions were subjected to isoelectric focusing analysis, which showed that purified chloroplast envelopes contain an NAD-MDH isoform tightly bound to the membranes, since treatment with 0.5 or 1% Triton X-100 was not able to release the enzyme from the envelopes.
  • In contrast, plasma membranes released an isoform with a pI of 3.5 following treatment with 0.5% Triton X-100.
  • The most abundant soluble leaf isoform had a pI of 9, while the chloroplast stroma contained an isoform with a pI of 5.3.
  • Kinetic analysis of oxaloacetate (OAA)-dependent NADH oxidation in different fractions gave different Km values for both substrates, the envelope- and plasma membrane-bound NAD-MDH exhibiting the highest affinities for OAA.
  • Our results indicate that the chloroplast envelope contains a specifically attached NAD-MDH isoform that could provide direct coupling between chloroplast and cytosol adenylate pools.
  • [MeSH-minor] Biomarkers / metabolism. Hydrogen-Ion Concentration. Isoenzymes / metabolism. Kinetics. NAD. Subcellular Fractions / enzymology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18239847.001).
  • [ISSN] 0033-183X
  • [Journal-full-title] Protoplasma
  • [ISO-abbreviation] Protoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Isoenzymes; 0U46U6E8UK / NAD; EC 1.1.1.37 / Malate Dehydrogenase
  •  go-up   go-down


40. Ying W: NAD+ and NADH in brain functions, brain diseases and brain aging. Front Biosci; 2007;12:1863-88
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+ and NADH in brain functions, brain diseases and brain aging.
  • Numerous studies have suggested that NAD+ and NADH mediate multiple major biological processes, including calcium homeostasis, energy metabolism, mitochondrial functions, cell death and aging.
  • In particular, NAD+ and NADH have emerged as novel, fundamental regulators of calcium homeostasis.
  • It appears that most of the components in the metabolic pathways of NAD+ and NADH, including poly(ADP-ribose), ADP-ribose, cyclic ADP-ribose, O-acetyl-ADP-ribose, nicotinamide and kynurenine, can produce significant biological effects.
  • This exquisiteness of NAD+ and NADH metabolism could epitomize the exquisiteness of life, through which we may grasp the intrinsic harmony life has evolved to produce.
  • The exquisiteness also suggests a central regulatory role of NAD+ and NADH in life.
  • It is tempted to propose that NAD+ and NADH, together with ATP and Ca2+, constitute a Central Regulatory Network of life.
  • Increasing evidence has also suggested that NAD+ and NADH play important roles in multiple biological processes in brains, such as neurotransmission and learning and memory.
  • NAD+ and NADH may also mediate brain aging and the tissue damage in various brain illnesses.
  • Our latest studies have suggested that NADH can be transported across the plasma membranes of astrocytes, and that NAD+ administration can markedly decrease ischemic brain injury.
  • Based on this information, it is proposed that NAD+ and NADH are fundamental mediators of brain functions, brain senescence and multiple brain diseases.
  • Because numerous properties of NAD+ and NADH remain unclear, future studies regarding NAD+ and NADH may expose some fundamental mechanisms underlying brain functions, brain pathologies and brain aging.
  • [MeSH-major] Aging / physiology. Brain / physiology. Brain Diseases / etiology. NAD / physiology

  • MedlinePlus Health Information. consumer health - Brain Diseases.
  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17127427.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD
  • [Number-of-references] 282
  •  go-up   go-down


41. Denu JM: Vitamins and aging: pathways to NAD+ synthesis. Cell; 2007 May 4;129(3):453-4
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vitamins and aging: pathways to NAD+ synthesis.
  • Recent genetic evidence reveals additional salvage pathways for NAD(+) synthesis.
  • In this issue, Belenky et al. (2007) report that nicotinamide riboside, a new NAD(+) precursor, regulates Sir2 deacetylase activity and life span in yeast.
  • The ability of nicotinamide riboside to enhance life span does not depend on calorie restriction.
  • [MeSH-major] Aging / metabolism. Histone Deacetylases / metabolism. NAD / biosynthesis. Niacinamide / analogs & derivatives. Saccharomyces cerevisiae / metabolism. Silent Information Regulator Proteins, Saccharomyces cerevisiae / metabolism. Sirtuins / metabolism. Vitamins / metabolism

  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Cell. 2007 May 4;129(3):473-84 [17482543.001]
  • (PMID = 17482537.001).
  • [ISSN] 0092-8674
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Silent Information Regulator Proteins, Saccharomyces cerevisiae; 0 / Vitamins; 0U46U6E8UK / NAD; 1341-23-7 / nicotinamide-beta-riboside; 25X51I8RD4 / Niacinamide; EC 3.5.1.- / SIR2 protein, S cerevisiae; EC 3.5.1.- / Sirtuin 2; EC 3.5.1.- / Sirtuins; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


42. Dudev T, Lim C: Factors controlling the mechanism of NAD(+) non-redox reactions. J Am Chem Soc; 2010 Nov 24;132(46):16533-43
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Factors controlling the mechanism of NAD(+) non-redox reactions.
  • β-Nicotinamide adenine dinucleotide (NAD(+)) is an indispensable coenzyme or substrate for enzymes involved in catalyzing redox and non-redox reactions.
  • ADP-ribosylating enzymes catalyze cleavage of the nicotinamide-glycosyl bond of NAD(+) and addition of a nucleophilic group from their substrate proteins to the N-ribose anomeric carbon of NAD(+).
  • Although the role of the nicotinamide-ribose fragment in the mechanism of NAD(+) hydrolysis has been examined, the role of the doubly negatively charged, flexible, and chemically reactive NAD(+) diphosphate moiety in the reaction process has largely been neglected.
  • In this study, we endeavor to fill in these gaps and elucidate the role of these factors in controlling the NAD(+) nicotinamide-glycosyl bond cleavage.
  • Using density functional theory combined with continuum dielectric methods, we modeled both S(N)1 and S(N)2 reaction pathways and assessed the role of the diphosphate group in stabilizing the (i) NAD(+) ground state, (ii) oxocarbocation intermediate, (iii) reaction product, and (iv) nucleophile.
  • [MeSH-major] NAD / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21047075.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD
  •  go-up   go-down


43. Ma B, Pan SJ, Zupancic ML, Cormack BP: Assimilation of NAD(+) precursors in Candida glabrata. Mol Microbiol; 2007 Oct;66(1):14-25
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assimilation of NAD(+) precursors in Candida glabrata.
  • The yeast pathogen Candida glabrata is a nicotinamide adenine dinucleotide (NAD(+)) auxotroph and its growth depends on the environmental supply of vitamin precursors of NAD(+). C. glabrata salvage pathways defined in this article allow NAD(+) to be synthesized from three compounds - nicotinic acid (NA), nicotinamide (NAM) and nicotinamide riboside (NR).
  • The second is a novel pathway in which NR is degraded by the nucleosidases Pnp1 and Urh1, with a minor role for Meu1, and ultimately converted to NAD(+) via the nicotinamidase Pnc1 and the Preiss-Handler pathway.
  • Using C. glabrata mutants whose growth depends exclusively on the external NA or NR supply, we also show that C. glabrata utilizes NR and to a lesser extent NA as NAD(+) sources during disseminated infection.
  • [MeSH-major] Candida glabrata / metabolism. Metabolic Networks and Pathways. NAD / biosynthesis

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NICOTINIC ACID .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17725566.001).
  • [ISSN] 0950-382X
  • [Journal-full-title] Molecular microbiology
  • [ISO-abbreviation] Mol. Microbiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 2P01DK49720; United States / NIAID NIH HHS / AI / 5R01AI046223-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 1341-23-7 / nicotinamide-beta-riboside; 25X51I8RD4 / Niacinamide; 2679MF687A / Niacin; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / nicotinamide riboside kinase; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.5.1.19 / Nicotinamidase
  •  go-up   go-down


44. Poncet-Montange G, Assairi L, Arold S, Pochet S, Labesse G: NAD kinases use substrate-assisted catalysis for specific recognition of NAD. J Biol Chem; 2007 Nov 23;282(47):33925-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD kinases use substrate-assisted catalysis for specific recognition of NAD.
  • Here we describe the crystal structures of the NAD kinase (LmNADK1) from Listeria monocytogenes in complex with its substrate NAD, its product NADP, or two synthesized NAD mimics.
  • We identified one of the NAD mimics, di-adenosine diphosphate, as a new substrate for LmNADK1, whereas we showed that the closely related compound di-5'-thioadenosine is a novel non-natural inhibitor for this enzyme.
  • Indeed, sequence/structure comparison and directed mutagenesis have previously shown that NAD kinases (NADKs) and the distantly related 6-phosphofructokinases share the same catalytically important GGDGT motif.
  • Although this acidic residue chelates the catalytic Mg(2+) ion in 6-phosphofructokinases, it activates the phospho-acceptor (NAD) in NADKs.
  • [MeSH-minor] Amino Acid Motifs / genetics. Amino Acid Substitution. Aspartic Acid / chemistry. Aspartic Acid / genetics. Aspartic Acid / metabolism. Catalysis. Crystallography, X-Ray. Diacylglycerol Kinase / chemistry. Diacylglycerol Kinase / genetics. Diacylglycerol Kinase / metabolism. Magnesium / chemistry. Magnesium / metabolism. Mutation, Missense. NAD / chemistry. NAD / metabolism. Phosphofructokinase-1 / chemistry. Phosphofructokinase-1 / genetics. Phosphofructokinase-1 / metabolism. Structure-Activity Relationship. Substrate Specificity / genetics

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. MAGNESIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17686780.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2I1W/ 2I29/ 2I2A/ 2I2B/ 2I2C/ 2I2D/ 2I2E/ 2I2F/ 2Q5F
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0U46U6E8UK / NAD; 30KYC7MIAI / Aspartic Acid; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase; EC 2.7.1.107 / Diacylglycerol Kinase; EC 2.7.1.11 / Phosphofructokinase-1; EC 2.7.1.23 / NAD kinase; I38ZP9992A / Magnesium
  •  go-up   go-down


45. Benarroch D, Shuman S: Characterization of mimivirus NAD+-dependent DNA ligase. Virology; 2006 Sep 15;353(1):133-43
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of mimivirus NAD+-dependent DNA ligase.
  • Here we produced, purified, and characterized mimivirus DNA ligase (MimiLIG), an NAD+-dependent nick joining enzyme homologous to bacterial LigA and entomopoxvirus DNA ligase.
  • MimiLIG is a 636-aa polypeptide composed of an N-terminal NAD+ specificity module (domain Ia), linked to nucleotidyltransferase, OB-fold, helix-hairpin-helix, and BRCT domains, but it lacks the tetracysteine Zn-binding module found in all bacterial LigA enzymes.
  • MimiLIG requires conserved domain Ia residues Tyr36, Asp46, Tyr49, and Asp50 for its initial reaction with NAD+ to form the ligase-AMP intermediate, but not for the third step of phosphodiester formation at a preadenylylated nick.
  • The DeltaBRCT mutant of MimiLIG was impaired in sealing at a preadenylylated nick.
  • We propose that eukaryal DNA viruses acquired the NAD+-dependent ligases by horizontal transfer from a bacterium and that MimiLIG predates entomopoxvirus ligase, which lacks both the tetracysteine and BRCT domains.
  • We speculate that the dissemination of NAD+-dependent ligase from bacterium to eukaryotic virus might have occurred within an amoebal host.

  • Hazardous Substances Data Bank. CYSTEINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16844179.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; EC 6.5.1.- / DNA Ligases; EC 6.5.1.2 / DNA ligase (NAD); K848JZ4886 / Cysteine
  •  go-up   go-down


46. Borradaile NM, Pickering JG: NAD(+), sirtuins, and cardiovascular disease. Curr Pharm Des; 2009;15(1):110-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD(+), sirtuins, and cardiovascular disease.
  • The sirtuin (SIRT) family of NAD(+)-dependent protein deacetylases and ADP-ribosyltransferases have emerged as exciting targets for CVD management that can impact the cardiovascular system both directly and indirectly, the latter by modulating whole body metabolism.
  • SIRT1-4 regulate the activities of a variety of transcription factors, coregulators, and enzymes that improve metabolic control in adipose tissue, liver, skeletal muscle, and pancreas, particularly during obesity and aging.
  • Because SIRT activity depends on cellular NAD+ availability, enzymes involved in NAD+ biosynthesis, including nicotinamide phosphoribosyltransferase (Nampt), may also be valuable pharmaceutical targets for managing CVD.
  • Herein we review the actions of the SIRT proteins on the cardiovascular system and consider the potential of modulating SIRT activity and NAD+ availability to control CVD.
  • [MeSH-major] Cardiovascular Diseases / metabolism. NAD / metabolism. Sirtuins / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19149606.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0U46U6E8UK / NAD; EC 3.5.1.- / Sirtuins
  • [Number-of-references] 100
  •  go-up   go-down


47. Wang J, He Z: NAD and axon degeneration: from the Wlds gene to neurochemistry. Cell Adh Migr; 2009 Jan-Mar;3(1):77-87

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD and axon degeneration: from the Wlds gene to neurochemistry.
  • The phenotype is attributed to the overexpression of a chimeric protein Wlds which contains a short fragment of the ubiquitin assembly protein UFD2 and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme Nicotinamide mononucleotide adenylyl-transferase-1 (Nmnat-1).
  • Together with a significant number of subsequential reports, this finding highlighted the substantial role of nicotinamide adenine dinucleotide (NAD) in the process of axon degeneration.
  • Here we reviewed the history of axon degeneration research from a neurochemical standpoint and discuss the potential involvement of NAD synthesis, NAD consumption and NAD-dependent proteins and small molecules in axon degeneration.
  • [MeSH-major] Axons / pathology. NAD / metabolism. Nerve Tissue Proteins / genetics. Nervous System / metabolism. Nervous System / pathology. Wallerian Degeneration / metabolism. Wallerian Degeneration / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2006 Aug 16;26(33):8484-91 [16914673.001]
  • [Cites] J Neurosci. 2006 Sep 20;26(38):9794-804 [16988050.001]
  • [Cites] Eur J Neurosci. 2006 Oct;24(8):2163-8 [17074042.001]
  • [Cites] J Neurosci Res. 2006 Dec;84(8):1799-807 [17022038.001]
  • [Cites] Cell Death Differ. 2007 Jan;14(1):116-27 [16645633.001]
  • [Cites] PLoS Biol. 2006 Nov;4(12):e416 [17132048.001]
  • [Cites] Annu Rev Neurosci. 2005;28:127-56 [16022592.001]
  • [Cites] J Cell Biol. 2005 Aug 1;170(3):349-55 [16043516.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36334-41 [16118205.001]
  • [Cites] Mol Biol Cell. 2006 Mar;17(3):1075-84 [16371511.001]
  • [Cites] Neuron. 2006 Jun 15;50(6):869-81 [16772169.001]
  • [Cites] Neuron. 2006 Jun 15;50(6):883-95 [16772170.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):406-12 [11027696.001]
  • [Cites] FEBS Lett. 2001 Mar 9;492(1-2):95-100 [11248244.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):7225-32 [11063748.001]
  • [Cites] Bioessays. 2001 Jun;23(6):543-8 [11385634.001]
  • [Cites] Nature. 2001 Jul 26;412(6845):449-52 [11473321.001]
  • [Cites] J Physiol. 2001 Aug 1;534(Pt 3):627-39 [11483696.001]
  • [Cites] Neuron. 2001 Sep 27;31(6):957-71 [11580896.001]
  • [Cites] J Biotechnol. 2001 Dec 28;92(2):81-7 [11640979.001]
  • [Cites] Cell. 2001 Oct 19;107(2):137-48 [11672522.001]
  • [Cites] Cell. 2001 Oct 19;107(2):149-59 [11672523.001]
  • [Cites] Ann Neurol. 2001 Dec;50(6):773-9 [11761475.001]
  • [Cites] Nat Neurosci. 2001 Dec;4(12):1199-206 [11770485.001]
  • [Cites] Neuron. 2001 Dec 20;32(6):1013-26 [11754834.001]
  • [Cites] Gene. 2002 Feb 6;284(1-2):23-9 [11891043.001]
  • [Cites] Science. 2002 May 3;296(5569):868-71 [11988563.001]
  • [Cites] Neurosci Lett. 2002 Aug 9;328(2):150-4 [12133577.001]
  • [Cites] J Neurochem. 2001 Jan;76(2):321-31 [11208895.001]
  • [Cites] J Cell Biol. 2002 Aug 19;158(4):647-57 [12186850.001]
  • [Cites] J Physiol. 2002 Sep 15;543(Pt 3):739-55 [12231635.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):835-40 [12359228.001]
  • [Cites] Cell. 2002 Oct 18;111(2):209-18 [12408865.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45099-107 [12297502.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jan 10;300(2):297-304 [12504083.001]
  • [Cites] Eur J Immunol. 2002 Nov;32(11):3225-34 [12555668.001]
  • [Cites] J Biol Chem. 2003 Apr 11;278(15):13503-11 [12574164.001]
  • [Cites] J Neurochem. 2003 Jun;85(5):1148-58 [12753074.001]
  • [Cites] Bioessays. 2003 Jul;25(7):683-90 [12815723.001]
  • [Cites] Neuron. 2003 Jun 19;38(6):871-85 [12818174.001]
  • [Cites] Neuron. 2003 Jul 17;39(2):217-25 [12873380.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7436-42 [14612543.001]
  • [Cites] Neurochem Int. 2004 Apr;44(5):361-9 [14643754.001]
  • [Cites] Cell. 2004 Feb 20;116(4):551-63 [14980222.001]
  • [Cites] Science. 2004 Mar 26;303(5666):2011-5 [14976264.001]
  • [Cites] Anal Biochem. 2004 Sep 1;332(1):90-9 [15301953.001]
  • [Cites] Science. 2004 Aug 13;305(5686):1010-3 [15310905.001]
  • [Cites] J Biol Chem. 1966 Jan 10;241(1):188-91 [4285133.001]
  • [Cites] Biochim Biophys Acta. 1971 Apr 29;238(1):82-5 [4325158.001]
  • [Cites] J Biol Chem. 1989 Jan 25;264(3):1608-15 [2912976.001]
  • [Cites] J Neuropathol Exp Neurol. 1991 May;50(3):192-204 [2022963.001]
  • [Cites] Biochem Pharmacol. 1992 Sep 1;44(5):947-53 [1530662.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9717-20 [8415768.001]
  • [Cites] Mol Cell Endocrinol. 1994 Jan;98(2):125-31 [8143921.001]
  • [Cites] Eur J Neurosci. 1994 Apr 1;6(4):516-24 [8025707.001]
  • [Cites] Dev Biol. 1994 Sep;165(1):63-72 [8088451.001]
  • [Cites] J Neurocytol. 1995 May;24(5):333-40 [7650538.001]
  • [Cites] J Neurosci. 1995 Oct;15(10):6445-52 [7472407.001]
  • [Cites] Biochimie. 1995;77(5):394-8 [8527495.001]
  • [Cites] Trends Neurosci. 1995 Nov;18(11):489-96 [8592758.001]
  • [Cites] Neurosci Lett. 1995 Oct 27;199(3):163-6 [8577388.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3699-705 [8631983.001]
  • [Cites] J Neurochem. 1996 Sep;67(3):1259-67 [8752134.001]
  • [Cites] Exp Cell Res. 1999 Jun 15;249(2):396-403 [10366439.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jun 24;260(1):273-9 [10381378.001]
  • [Cites] Nat Genet. 1999 Sep;23(1):47-51 [10471497.001]
  • [Cites] J Physiol. 1960 Jan;150:145-68 [13800902.001]
  • [Cites] Science. 2005 Feb 25;307(5713):1282-8 [15731448.001]
  • [Cites] Mol Cell Neurosci. 2005 Mar;28(3):430-9 [15737734.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Aug 3;359(3):665-71 [17560549.001]
  • [Cites] Nature. 2008 Apr 17;452(7189):887-91 [18344983.001]
  • [Cites] Biochem J. 1996 Oct 15;319 ( Pt 2):613-7 [8912702.001]
  • [Cites] Biochem J. 1997 Mar 15;322 ( Pt 3):909-17 [9148768.001]
  • [Cites] Nature. 1998 Sep 24;395(6700):395-8 [9759731.001]
  • [Cites] Free Radic Biol Med. 1998 Oct;25(6):694-702 [9801070.001]
  • [Cites] Mol Cell Neurosci. 1999 Sep;14(3):180-98 [10576889.001]
  • [Cites] J Neurosci. 2000 Feb 15;20(4):1333-41 [10662823.001]
  • [Cites] Nature. 2000 Feb 17;403(6771):795-800 [10693811.001]
  • [Cites] Eur J Biochem. 2000 Mar;267(6):1550-64 [10712584.001]
  • [Cites] Prog Neurobiol. 2000 Oct;62(3):273-95 [10840150.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11377-82 [11027338.001]
  • [Cites] Science. 2000 Dec 1;290(5497):1717-21 [11099404.001]
  • [Cites] Acta Neuropathol. 1971;5:Suppl 5:3-16 [5562691.001]
  • [Cites] J Neural Transm. 1978;42(1):37-43 [641543.001]
  • [Cites] Eur J Biochem. 1987 Apr 1;164(1):197-203 [3830181.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 May;84(10):3491-5 [3472219.001]
  • [Cites] Genetics. 1987 May;116(1):9-22 [3297920.001]
  • [Cites] Toxicology. 1987 Oct 30;46(2):125-39 [3313811.001]
  • [Cites] Exp Cell Res. 1988 Jul;177(1):103-8 [3391236.001]
  • [Cites] Nat Med. 2005 May;11(5):572-7 [15821747.001]
  • [Cites] Neuron. 2003 Oct 9;40(2):401-13 [14556717.001]
  • (PMID = 19372760.001).
  • [ISSN] 1933-6926
  • [Journal-full-title] Cell adhesion & migration
  • [ISO-abbreviation] Cell Adh Migr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0U46U6E8UK / NAD
  • [Number-of-references] 94
  • [Other-IDs] NLM/ PMC2675153
  •  go-up   go-down


48. Vilchèze C, Weisbrod TR, Chen B, Kremer L, Hazbón MH, Wang F, Alland D, Sacchettini JC, Jacobs WR Jr: Altered NADH/NAD+ ratio mediates coresistance to isoniazid and ethionamide in mycobacteria. Antimicrob Agents Chemother; 2005 Feb;49(2):708-20
Hazardous Substances Data Bank. ISONIAZID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered NADH/NAD+ ratio mediates coresistance to isoniazid and ethionamide in mycobacteria.
  • All mutants had defects in NdhII activity resulting in an increase in intracellular NADH/NAD(+) ratios.
  • Increasing NADH levels were shown to protect InhA against inhibition by the INH-NAD adduct formed upon INH activation.
  • We conclude that ndh mutations mediate a novel mechanism of resistance by increasing the NADH cellular concentration, which competitively inhibits the binding of INH-NAD or ETH-NAD adduct to InhA.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETHIONAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Antimicrob Agents Chemother. 2000 Jan;44(1):103-10 [10602730.001]
  • [Cites] J Biol Chem. 2003 Jun 6;278(23):20547-54 [12654922.001]
  • [Cites] J Bacteriol. 2000 Jul;182(14):4059-67 [10869086.001]
  • [Cites] Tuber Lung Dis. 2000;80(1):47-56 [10897383.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9677-82 [10944230.001]
  • [Cites] J Biol Chem. 2000 Sep 8;275(36):28326-31 [10869356.001]
  • [Cites] J Bacteriol. 2000 Dec;182(24):6884-91 [11092846.001]
  • [Cites] Biochim Biophys Acta. 2000 Aug 15;1459(2-3):274-83 [11004440.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Jul;45(7):2157-9 [11408244.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):12824-9 [11823459.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Dec;47(12):3799-805 [14638486.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):13881-6 [14623976.001]
  • [Cites] J Biol Chem. 2004 Jan 30;279(5):3354-60 [14610090.001]
  • [Cites] J Clin Microbiol. 2004 Mar;42(3):1294-5 [15004099.001]
  • [Cites] Am Rev Respir Dis. 1965 Nov;92(5):687-703 [5321145.001]
  • [Cites] Tubercle. 1966 Jun;47(2):198-206 [4960414.001]
  • [Cites] Rev Tuberc Pneumol (Paris). 1967 Jun;31(4):433-74 [4974609.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] Antimicrob Agents Chemother. 1972 Jul;2(1):29-35 [4208567.001]
  • [Cites] Am Rev Respir Dis. 1964 Sep;90:468-9 [14215919.001]
  • [Cites] Biochemistry. 1981 Jun 9;20(12):3621-8 [7020757.001]
  • [Cites] Biochemistry. 1987 Dec 1;26(24):7732-7 [3122832.001]
  • [Cites] FEBS Lett. 1991 Feb 11;279(1):5-8 [1995341.001]
  • [Cites] Nature. 1991 Jun 6;351(6326):456-60 [1904554.001]
  • [Cites] Nature. 1992 Aug 13;358(6387):591-3 [1501713.001]
  • [Cites] Biochim Biophys Acta. 1993 Feb 8;1141(1):1-17 [8435434.001]
  • [Cites] J Bacteriol. 1993 May;175(10):3020-5 [8491720.001]
  • [Cites] Mol Microbiol. 1993 May;8(3):521-4 [8392139.001]
  • [Cites] Science. 1994 Jan 14;263(5144):227-30 [8284673.001]
  • [Cites] Lancet. 1994 Jul 30;344(8918):293-8 [7914261.001]
  • [Cites] Mol Microbiol. 1994 May;12(3):433-44 [8065261.001]
  • [Cites] Mol Microbiol. 1994 Jul;13(2):172-82 [7984099.001]
  • [Cites] Science. 1995 Mar 17;267(5204):1638-41 [7886450.001]
  • [Cites] Biochemistry. 1995 Jul 4;34(26):8235-41 [7599116.001]
  • [Cites] J Bacteriol. 1996 Oct;178(20):6013-8 [8830700.001]
  • [Cites] Science. 1998 Jan 2;279(5347):98-102 [9417034.001]
  • [Cites] J Bacteriol. 1998 May;180(9):2459-67 [9573199.001]
  • [Cites] Biochim Biophys Acta. 1998 May 6;1364(2):125-33 [9593856.001]
  • [Cites] J Infect Dis. 1998 Sep;178(3):769-75 [9728546.001]
  • [Cites] Proc Int Conf Intell Syst Mol Biol. 1998;6:175-82 [9783223.001]
  • [Cites] Infect Immun. 1998 Nov;66(11):5099-106 [9784509.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Mar;43(3):711-3 [10049298.001]
  • [Cites] Science. 1952 Aug 8;116(3006):129-34 [14950210.001]
  • [Cites] Metab Eng. 2002 Apr;4(2):182-92 [12009797.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Jul;46(7):2137-44 [12069966.001]
  • [Cites] Mol Microbiol. 2002 Oct;46(2):453-66 [12406221.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Apr;47(4):1241-50 [12654653.001]
  • [Cites] Arch Intern Med. 2003 May 12;163(9):1009-21 [12742798.001]
  • [Cites] Tuberculosis (Edinb). 2003;83(1-3):44-51 [12758188.001]
  • [Cites] J Biol Chem. 2000 Jan 28;275(4):2520-6 [10644708.001]
  • (PMID = 15673755.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI043268; United States / NIAID NIH HHS / AI / AI46669; United States / NIAID NIH HHS / AI / R01 AI043268; United States / NIAID NIH HHS / AI / R01 AI046669; United States / NIAID NIH HHS / AI / AI43268
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / Culture Media; 0U46U6E8UK / NAD; EC 1.6.99.- / Quinone Reductases; EC 1.6.99.3 / NADH Dehydrogenase; EC 1.6.99.5 / NADH dehydrogenase (quinone); OAY8ORS3CQ / Ethionamide; V83O1VOZ8L / Isoniazid
  • [Other-IDs] NLM/ PMC547332
  •  go-up   go-down


49. Olesen UH, Christensen MK, Björkling F, Jäättelä M, Jensen PB, Sehested M, Nielsen SJ: Anticancer agent CHS-828 inhibits cellular synthesis of NAD. Biochem Biophys Res Commun; 2008 Mar 21;367(4):799-804
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anticancer agent CHS-828 inhibits cellular synthesis of NAD.
  • Nicotinamide adenine dinucleotide (NAD) is required for both processes and is also continuously degraded by cellular enzymes.
  • Nicotinamide phosphoribosyltransferase (Nampt) is a crucial factor in the resynthesis of NAD, and thus in cancer cell survival.
  • Here, we establish the cytotoxic mechanism of action of the small molecule inhibitor CHS-828 to result from impaired synthesis of NAD.
  • Initially, we detected cross-resistance in cells between CHS-828 and a known inhibitor of Nampt, FK866, a compound of a structurally different class.
  • We then showed that nicotinamide protects against CHS-828-mediated cytotoxicity.
  • Finally, we observed that treatment with CHS-828 depletes cellular NAD levels in sensitive cancer cells.
  • In conclusion, these results strongly suggest that, like FK866, CHS-828 kills cancer cells by depleting NAD.
  • [MeSH-major] Acrylamides / administration & dosage. Antineoplastic Agents / administration & dosage. Apoptosis / drug effects. Cyanides / administration & dosage. Guanidines / administration & dosage. Lung Neoplasms / metabolism. NAD / metabolism. Piperidines / administration & dosage. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18201551.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cyanides; 0 / Guanidines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / N-(6-chlorophenoxyhexyl)-N''-cyano-N''-4-pyridylguanidine; 0 / Piperidines; 0U46U6E8UK / NAD
  •  go-up   go-down


50. Gerdes SY, Kurnasov OV, Shatalin K, Polanuyer B, Sloutsky R, Vonstein V, Overbeek R, Osterman AL: Comparative genomics of NAD biosynthesis in cyanobacteria. J Bacteriol; 2006 Apr;188(8):3012-23
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative genomics of NAD biosynthesis in cyanobacteria.
  • Biosynthesis of NAD(P) cofactors is of special importance for cyanobacteria due to their role in photosynthesis and respiration.
  • Despite significant progress in understanding NAD(P) biosynthetic machinery in some model organisms, relatively little is known about its implementation in cyanobacteria.
  • A detailed reconstruction of the NAD(P) metabolic subsystem using the SEED genomic platform (http://theseed.uchicago.edu/FIG/index.cgi) helped us accurately annotate respective genes in the entire set of 13 cyanobacterial species with completely sequenced genomes available at the time.
  • Comparative analysis of operational variants implemented in this divergent group allowed us to elucidate both conserved (de novo and universal pathways) and variable (recycling and salvage pathways) aspects of this subsystem.
  • Focused genetic and biochemical experiments confirmed several conjectures about the key aspects of this subsystem. (i) The product of the slr1691 gene, a homolog of Escherichia coli gene nadE containing an additional nitrilase-like N-terminal domain, is a NAD synthetase capable of utilizing glutamine as an amide donor in vitro. (ii) The product of the sll1916 gene, a homolog of E. coli gene nadD, is a nicotinic acid mononucleotide-preferring adenylyltransferase.
  • This gene is essential for survival and cannot be compensated for by an alternative nicotinamide mononucleotide (NMN)-preferring adenylyltransferase (slr0787 gene). (iii) The product of the slr0788 gene is a nicotinamide-preferring phosphoribosyltransferase involved in the first step of the two-step non-deamidating utilization of nicotinamide (NMN shunt). (iv) The physiological role of this pathway encoded by a conserved gene cluster, slr0787-slr0788, is likely in the recycling of endogenously generated nicotinamide, as supported by the inability of this organism to utilize exogenously provided niacin.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Glutamine .
  • Hazardous Substances Data Bank. NICOTINIC ACID .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Soc Trans. 1996 Aug;24(3):729-33 [8878835.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5125-34 [8895556.001]
  • [Cites] DNA Res. 1996 Jun 30;3(3):109-36 [8905231.001]
  • [Cites] Science. 1997 Sep 5;277(5331):1453-62 [9278503.001]
  • [Cites] Gene. 1997 Sep 15;197(1-2):GC11-26 [9332394.001]
  • [Cites] J Bacteriol. 1997 Dec;179(24):7718-23 [9401030.001]
  • [Cites] Nucleic Acids Res. 2005;33(17):5691-702 [16214803.001]
  • [Cites] Nature. 2003 Aug 28;424(6952):1042-7 [12917642.001]
  • [Cites] Mol Microbiol. 2003 Sep;49(6):1577-93 [12950922.001]
  • [Cites] Trends Biotechnol. 2003 Nov;21(11):504-11 [14573364.001]
  • [Cites] DNA Res. 2003 Aug 31;10(4):137-45 [14621292.001]
  • [Cites] Cell Mol Life Sci. 2004 Jan;61(1):19-34 [14704851.001]
  • [Cites] J Struct Biol. 1999 Oct;127(3):279-82 [10544053.001]
  • [Cites] Eur J Biochem. 2000 Mar;267(6):1550-64 [10712584.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6658-63 [10841563.001]
  • [Cites] J Mol Microbiol Biotechnol. 1999 Aug;1(1):127-8 [10941793.001]
  • [Cites] J Bacteriol. 2001 Jan;183(1):292-300 [11114929.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):406-12 [11027696.001]
  • [Cites] Vitam Horm. 2001;61:103-19 [11153263.001]
  • [Cites] Methods Enzymol. 2001;330:134-57 [11210495.001]
  • [Cites] J Bacteriol. 2001 Feb;183(4):1168-74 [11157928.001]
  • [Cites] Mol Microbiol. 2001 Jun;40(6):1241-8 [11442824.001]
  • [Cites] In Silico Biol. 1999;1(2):93-108 [11471247.001]
  • [Cites] DNA Res. 2001 Oct 31;8(5):205-13; 227-53 [11759840.001]
  • [Cites] Science. 2002 Mar 8;295(5561):1895-7 [11847309.001]
  • [Cites] Int J Med Microbiol. 2002 Feb;291(6-7):523-9 [11890553.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):13148-54 [11788603.001]
  • [Cites] Plant Mol Biol. 2002 May;49(1):107-18 [12008895.001]
  • [Cites] Proteins. 2002 Jul 1;48(1):1-14 [12012333.001]
  • [Cites] J Bacteriol. 2002 Aug;184(16):4555-72 [12142426.001]
  • [Cites] Protein Expr Purif. 2002 Aug;25(3):547-57 [12182838.001]
  • [Cites] J Biol Chem. 2002 Sep 6;277(36):33291-9 [12068016.001]
  • [Cites] DNA Res. 2002 Aug 31;9(4):123-30 [12240834.001]
  • [Cites] J Bacteriol. 2002 Dec;184(24):6906-17 [12446641.001]
  • [Cites] Science. 2002 Nov 22;298(5598):1616-20 [12446909.001]
  • [Cites] Trends Biochem Sci. 2003 Jan;28(1):41-8 [12517451.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 1;31(1):164-71 [12519973.001]
  • [Cites] Eur J Immunol. 2002 Nov;32(11):3225-34 [12555668.001]
  • [Cites] J Biol Chem. 2003 Apr 11;278(15):13503-11 [12574164.001]
  • [Cites] Res Microbiol. 2003 Apr;154(3):157-64 [12706503.001]
  • [Cites] Bioessays. 2003 Jul;25(7):683-90 [12815723.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):10020-5 [12917486.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33049-55 [12771147.001]
  • [Cites] Nature. 2003 Aug 28;424(6952):1037-42 [12917641.001]
  • [Cites] Curr Opin Microbiol. 2004 Apr;7(2):115-9 [15063846.001]
  • [Cites] Curr Med Chem. 2004 Apr;11(7):873-85 [15078171.001]
  • [Cites] Methods Enzymol. 1985;113:297-302 [3003498.001]
  • [Cites] J Bacteriol. 1990 May;172(5):2313-9 [2110139.001]
  • [Cites] Genome Res. 1998 Mar;8(3):203-10 [9521924.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9699-704 [9689144.001]
  • [Cites] FEBS Lett. 1999 Feb 12;444(2-3):222-6 [10050763.001]
  • [Cites] Curr Opin Plant Biol. 1998 Jun;1(3):217-23 [10066592.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1999;73:135-82, xi [10218108.001]
  • [Cites] J Bacteriol. 1999 Jul;181(13):3994-4003 [10383967.001]
  • [Cites] Genetics. 1999 Aug;152(4):1299-305 [10430560.001]
  • [Cites] J Bacteriol. 1999 Sep;181(17):5509-11 [10464228.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):30540-9 [10521436.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50754-63 [15381699.001]
  • [Cites] Bioinformatics. 2005 Feb 1;21(3):293-306 [15347579.001]
  • [Cites] Res Microbiol. 2005 Mar;156(2):173-7 [15748981.001]
  • [Cites] Bioinformatics. 2005 Jun;21 Suppl 1:i478-86 [15961494.001]
  • [Cites] J Bacteriol. 1990 Jun;172(6):3138-45 [2160938.001]
  • [Cites] Arch Microbiol. 1992;157(4):336-42 [1590707.001]
  • [Cites] Mol Cell Biol. 1994 Feb;14(2):1431-7 [8289818.001]
  • [Cites] J Bacteriol. 1994 Jun;176(11):3400-2 [8195100.001]
  • [Cites] Biochemistry. 1994 Nov 22;33(46):13662-7 [7947774.001]
  • [Cites] J Bacteriol. 1995 Jun;177(12):3527-33 [7768863.001]
  • [Cites] Science. 1995 Jul 28;269(5223):496-512 [7542800.001]
  • [Cites] Biochemistry. 1995 Oct 17;34(41):13431-6 [7577930.001]
  • [Cites] Anal Biochem. 1995 Jun 10;228(1):64-8 [8572289.001]
  • (PMID = 16585762.001).
  • [ISSN] 0021-9193
  • [Journal-full-title] Journal of bacteriology
  • [ISO-abbreviation] J. Bacteriol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI059146; United States / NIAID NIH HHS / AI / 1R01 AI 059146-01A2
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0RH81L854J / Glutamine; 0U46U6E8UK / NAD; 1094-61-7 / Nicotinamide Mononucleotide; 25X51I8RD4 / Niacinamide; 2679MF687A / Niacin; 321-02-8 / nicotinate mononucleotide; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.7.7.- / Nucleotidyltransferases; EC 2.7.7.42 / glutamine-synthetase adenylyltransferase; EC 6.3.1.- / Amide Synthases; EC 6.3.1.5 / NAD+ synthase
  • [Other-IDs] NLM/ PMC1446974
  •  go-up   go-down


51. Lawson M, Uciechowska U, Schemies J, Rumpf T, Jung M, Sippl W: Inhibitors to understand molecular mechanisms of NAD(+)-dependent deacetylases (sirtuins). Biochim Biophys Acta; 2010 Oct-Dec;1799(10-12):726-39
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors to understand molecular mechanisms of NAD(+)-dependent deacetylases (sirtuins).
  • Unlike the other three of the four classes of HDACs that have been identified in humans, which are zinc-dependent amidohydrolases, class III HDACs depend on nicotinamide adenine dinucleotide (NAD(+)) for their catalytic activity.
  • [MeSH-major] Histone Deacetylase Inhibitors. NAD. Sirtuins

  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20601279.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0U46U6E8UK / NAD; EC 3.5.1.- / Sirtuins
  •  go-up   go-down


52. Adams JD Jr: Alzheimer's disease, ceramide, visfatin and NAD. CNS Neurol Disord Drug Targets; 2008 Dec;7(6):492-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alzheimer's disease, ceramide, visfatin and NAD.
  • A new mechanism for visfatin/NAD (nicotinamide adenine dinucleotide)-induced oxidative stress is presented involving redox cycling catalyzed by xanthine dehydrogenase and NADH oxidase.
  • [MeSH-major] Alzheimer Disease / metabolism. Ceramides / metabolism. NAD / metabolism. Nicotinamide Phosphoribosyltransferase / metabolism

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19128206.001).
  • [ISSN] 1996-3181
  • [Journal-full-title] CNS & neurological disorders drug targets
  • [ISO-abbreviation] CNS Neurol Disord Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Ceramides; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase
  • [Number-of-references] 67
  •  go-up   go-down


53. Koch-Nolte F, Haag F, Guse AH, Lund F, Ziegler M: Emerging roles of NAD+ and its metabolites in cell signaling. Sci Signal; 2009;2(57):mr1
Hazardous Substances Data Bank. NICOTINAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emerging roles of NAD+ and its metabolites in cell signaling.
  • Nicotinamide adenine dinucleotide (NAD(+)) is the universal currency of energy metabolism and electron transfer.
  • Recent studies indicate that apart from its role as a coenzyme, NAD(+) and its metabolites also function in cell signaling pathways; for example, they are substrates for nucleotide-metabolizing enzymes and ligands for extra- and intracellular receptors and ion channels.
  • Moreover, the NAD(+) and NAD(+) phosphate metabolites adenosine 5'-diphosphoribose (ADP-ribose), cyclic ADP-ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) have emerged as key second messengers in Ca(2+) signaling.
  • A symposium in Hamburg, Germany, brought together 120 researchers from various fields, who were all engaged in the molecular characterization of the key players of NAD(+) signaling (www.NAD2008.de).
  • [MeSH-major] Cell Physiological Phenomena. NAD / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Adenosine Diphosphate Ribose / metabolism. Animals. Energy Metabolism. Humans. NADP / metabolism. Niacinamide / metabolism. Second Messenger Systems / physiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19211509.001).
  • [ISSN] 1937-9145
  • [Journal-full-title] Science signaling
  • [ISO-abbreviation] Sci Signal
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 20762-30-5 / Adenosine Diphosphate Ribose; 25X51I8RD4 / Niacinamide; 53-59-8 / NADP
  • [Number-of-references] 50
  •  go-up   go-down


54. Fukuwatari T, Shibata K: Consideration of diurnal variations in human blood NAD and NADP concentrations. J Nutr Sci Vitaminol (Tokyo); 2009 Jun;55(3):279-81
Hazardous Substances Data Bank. NICOTINAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Consideration of diurnal variations in human blood NAD and NADP concentrations.
  • The sum of the urinary excretion of nicotinamide and its catabolites, which are metabolites of NAD and NADP, were observed to have clear diurnal variations in human urine.
  • Then, we examined whether NAD and NADP in blood also showed the diurnal variation.
  • In addition, we examined whether diurnal variations were affected by the intakes of dietary nicotinamide or not.
  • As a result, neither the NAD nor the NADP content of the blood shows the diurnal variation regardless of the administered amount of nicotinamide.
  • The concentrations of NAD and NADP did not increase according to the intake of nicotinamide.
  • The existence of a mechanism by which NAD and the NADP levels of the blood are constantly maintained by the adjustment of the amount of excretion to the urinary bladder, was suggested.
  • [MeSH-major] Circadian Rhythm / physiology. NAD / blood. NADP / blood

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19602837.001).
  • [ISSN] 1881-7742
  • [Journal-full-title] Journal of nutritional science and vitaminology
  • [ISO-abbreviation] J. Nutr. Sci. Vitaminol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 25X51I8RD4 / Niacinamide; 53-59-8 / NADP
  •  go-up   go-down


55. Li ZJ, Cai L, Wu Q, Chen GQ: Overexpression of NAD kinase in recombinant Escherichia coli harboring the phbCAB operon improves poly(3-hydroxybutyrate) production. Appl Microbiol Biotechnol; 2009 Jul;83(5):939-47
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of NAD kinase in recombinant Escherichia coli harboring the phbCAB operon improves poly(3-hydroxybutyrate) production.
  • NAD kinase was overexpressed to enhance the accumulation of poly(3-hydroxybutyrate) (PHB) in recombinant Escherichia coli harboring PHB synthesis pathway via an accelerated supply of NADPH, which is one of the most crucial factors influencing PHB production.
  • A high copy number expression plasmid pE76 led to a stronger NAD kinase activity than that brought about by the low copy number plasmid pELRY.
  • Overexpressing NAD kinase in recombinant E. coli was found not to have a negative effect on cell growth in the absence of PHB synthesis.
  • Shake flask experiments demonstrated that excess NAD kinase in E. coli harboring the PHB synthesis operon could increase the accumulation of PHB to 16-35 wt.
  • Although the two NAD kinase overexpression recombinants exhibited large disparity on NAD kinase activity, their influence on cell growth and PHB accumulation was not proportional.
  • Under the same growth conditions without process optimization, the NAD kinase-overexpressing recombinant produced 14 g/L PHB compared with 7 g/L produced by the control in a 28-h fermentor study.
  • In addition, substrate to PHB yield Y (PHB/glucose) showed an increase from 0.08 g PHB/g glucose for the control to 0.15 g PHB/g glucose for the NAD kinase-overexpressing strain, a 76% increase for the Y (PHB/glucose).
  • These results clearly showed that the overexpression of NAD kinase could be used to enhance the PHB synthesis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19357844.001).
  • [ISSN] 1432-0614
  • [Journal-full-title] Applied microbiology and biotechnology
  • [ISO-abbreviation] Appl. Microbiol. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Escherichia coli Proteins; 0 / Hydroxybutyrates; 0 / Polyesters; 26063-00-3 / poly-beta-hydroxybutyrate; 53-59-8 / NADP; EC 2.7.- / Phosphotransferases; EC 2.7.1.- / NadK protein, E coli
  •  go-up   go-down


56. Ying W: NAD+ and NADH in cellular functions and cell death. Front Biosci; 2006;11:3129-48
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+ and NADH in cellular functions and cell death.
  • Increasing evidence has indicated that NAD+ and NADH play critical roles not only in energy metabolism, but also in cell death and various cellular functions including regulation of calcium homeostasis and gene expression.
  • It has also been indicated that NAD+ and NADH are mediators of multiple major biological processes including aging.
  • NAD+ and NADH produce the biological effects by regulating numerous NAD+/NADH-dependent enzymes, including dehydrogenases, poly(ADP-ribose) polymerases, Sir2 family proteins (sirtuins), mono(ADP-ribosyl)transferases, and ADP-ribosyl cyclases.
  • Of particular interest, NAD+-dependent generation of ADP-ribose, cyclic ADP-ribose and O-acetyl-ADP-ribose can mediate calcium homeostasis by affecting TRPM2 receptors and ryanodine receptors; and sirtuins and PARPs appear to play key roles in aging, cell death and a variety of cellular functions.
  • It has also been indicated that NADH and NAD+ can be transported across plasma membranes of cells, and that extracellular NAD+ may be a new signaling molecule.
  • Our latest studies have shown that intranasal NAD+ administration can profoundly decrease ischemic brain damage.
  • These new pieces of information have fundamentally changed our understanding about NAD+ and NADH, suggesting novel paradigms about the metabolism and biological activities of NAD+ and NADH.
  • Based on this information, it is tempted to hypothesize that NAD+ and NADH, together with ATP and Ca2+, may be four most fundamental components in life, which can significantly affect nearly all major biological processes.
  • Future studies on NAD+ and NADH may not only elucidate some fundamental mysteries in biology, but also provide novel insights for interfering aging and many disease processes.
  • [MeSH-major] Cell Death. Cell Physiological Phenomena. NAD / biosynthesis. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16720381.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0U46U6E8UK / NAD; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 187
  •  go-up   go-down


57. Ying W: NAD+ and NADH in ischemic brain injury. Front Biosci; 2008;13:1141-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+ and NADH in ischemic brain injury.
  • NAD+ and NADH have been emerging as the common mediators of energy metabolism, mitochondrial functions, calcium homeostasis, aging and cell death.
  • NAD+ and NADH can affect cell death by various mechanisms, such as influencing energy metabolism, mitochondrial permeability transition pores, and apoptosis-inducing factor.
  • Because energy failure, calcium disregulation and cell death are the key components in the tissue damaging cascade initiated by cerebral ischemia, it is likely that NAD+ and NADH play significant roles in ischemic brain damage.
  • Many studies, including the findings that poly(ADP-ribose) polymerase-1 mediates ischemic brain injury and that NAD+ administration can decrease ischemic brain damage, have suggested significant roles of NAD+ and NADH in the debilitating illness.
  • However, there is still distinct insufficiency of the information regarding the roles of NAD+ and NADH in ischemic brain injury.
  • Because increasing evidence has indicated critical functions of NAD+ and NADH in various biological processes, future studies on the roles of NAD+ and NADH in cerebral ischemia may expose essential mechanisms underlying ischemic brain injury and suggest novel therapeutic strategies for the illness.
  • [MeSH-major] Brain Injuries / pathology. Brain Ischemia / metabolism. NAD / metabolism
  • [MeSH-minor] Animals. Apoptosis. Brain / metabolism. Brain / pathology. Cell Death. Humans. Ischemia. Ischemic Preconditioning. Models, Biological. Poly Adenosine Diphosphate Ribose / metabolism. Poly(ADP-ribose) Polymerases / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17981619.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 26656-46-2 / Poly Adenosine Diphosphate Ribose; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 135
  •  go-up   go-down


58. Ren X, Yang L, Tang F, Yan C, Ren J: Enzyme biosensor based on NAD-sensitive quantum dots. Biosens Bioelectron; 2010 Sep 15;26(1):271-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enzyme biosensor based on NAD-sensitive quantum dots.
  • In this system, the fluorescence intensities of the QDs are quenched by nicotinamide adenine dinucleotide (NAD, the coenzyme of LDH) first and then intensified with increasing amounts of the LDH because of the consumption of the NAD in the biocatalyzed reaction.
  • [MeSH-major] Biosensing Techniques / instrumentation. L-Lactate Dehydrogenase / chemistry. NAD / analysis. Quantum Dots. Spectrometry, Fluorescence / instrumentation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20627509.001).
  • [ISSN] 1873-4235
  • [Journal-full-title] Biosensors & bioelectronics
  • [ISO-abbreviation] Biosens Bioelectron
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0U46U6E8UK / NAD; EC 1.1.1.27 / L-Lactate Dehydrogenase
  •  go-up   go-down


59. Jauch R, Humm A, Huber R, Wahl MC: Structures of Escherichia coli NAD synthetase with substrates and products reveal mechanistic rearrangements. J Biol Chem; 2005 Apr 15;280(15):15131-40
Hazardous Substances Data Bank. (L)-Phenylalanine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structures of Escherichia coli NAD synthetase with substrates and products reveal mechanistic rearrangements.
  • Nicotinamide adenine dinucleotide synthetases (NADS) catalyze the amidation of nicotinic acid adenine dinucleotide (NAAD) to yield the enzyme cofactor nicotinamide adenine dinucleotide (NAD).
  • Here we describe the crystal structures of the ammonia-dependent homodimeric NADS from Escherichia coli alone and in complex with natural substrates and with the reaction product NAD.
  • The structures disclosed two NAAD/NAD binding sites at the dimer interface and an adenosine triphosphate (ATP) binding site within each subunit.
  • Comparison with the Bacillus subtilis NADS showed pronounced chemical differences in the NAAD/NAD binding sites and less prominent differences in the ATP binding pockets.
  • In addition, the E. coli NADS structures revealed unexpected dynamical rearrangements in the NAAD/NAD binding pocket upon NAAD-to-NAD conversion, which define a catalysis state and a substrate/product exchange state.
  • The two states are adopted by concerted movement of the nicotinysyl moieties of NAAD and NAD, Phe-170, and residues 224-228, which may be triggered by differential coordination of a magnesium ion to NAAD and NAD.
  • [MeSH-major] Amide Synthases / chemistry. Escherichia coli / enzymology. NAD / analogs & derivatives
  • [MeSH-minor] Adenosine Triphosphate / chemistry. Amino Acid Sequence. Bacillus subtilis / metabolism. Binding Sites. Cloning, Molecular. Crystallography, X-Ray. Dimerization. Humans. Models, Chemical. Models, Molecular. Molecular Sequence Data. Phenylalanine / chemistry. Phylogeny. Protein Conformation. Protein Structure, Secondary. Protein Structure, Tertiary. Sequence Homology, Amino Acid

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15699042.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 1WXE/ 1WXF/ 1WXG/ 1WXH/ 1WXI
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 47E5O17Y3R / Phenylalanine; 6450-77-7 / nicotinic acid adenine dinucleotide; 8L70Q75FXE / Adenosine Triphosphate; EC 6.3.1.- / Amide Synthases; EC 6.3.1.5 / NAD+ synthase
  •  go-up   go-down


60. Till S, Ladurner AG: Sensing NAD metabolites through macro domains. Front Biosci (Landmark Ed); 2009;14:3246-58
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensing NAD metabolites through macro domains.
  • Many macro domains, including those of the human histone macroH2A1.1, bind NAD metabolites such as ADP-ribose, suggesting that macro domains may function in the recognition of this and related molecules.
  • The presence of a metabolite-binding function in a repressive chromatin component opens new potential connections between chromosome structure, gene silencing and cellular metabolism.
  • Current evidence suggests that macro domains also represent a novel tool for studying NAD metabolites and may be an attractive drug target for the treatment of diseases.
  • [MeSH-major] NAD / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19273270.001).
  • [ISSN] 1093-4715
  • [Journal-full-title] Frontiers in bioscience (Landmark edition)
  • [ISO-abbreviation] Front Biosci (Landmark Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0U46U6E8UK / NAD; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 68
  •  go-up   go-down


61. Gimenes D, Constantin J, Comar JF, Kelmer-Bracht AM, Broetto-Biazon AC, Bracht A: Liver parenchyma heterogeneity in the response to extracellular NAD+. Cell Biochem Funct; 2006 Jul-Aug;24(4):313-25
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liver parenchyma heterogeneity in the response to extracellular NAD+.
  • The perfused rat liver responds intensely to NAD+ infusion (20-100 microM).
  • The aim of the present work was to investigate the distribution of the response to extracellular NAD+ along the hepatic acinus.
  • Various combinations of perfusion directions (antegrade and retrograde) and infusion routes (portal vein, hepatic vein and hepatic artery) were used in order to supply NAD+ to different regions of the liver parenchyma, also taking advantage of the fact that its extracellular transformation generates steep concentration gradients.
  • Oxygen uptake was stimulated by NAD+ in retrograde perfusion (irrespective of the infusion route) and transiently inhibited in antegrade perfusion.
  • Stimulation of glucose release was more intense when NAD+ was infused into the portal vein or into the hepatic artery, indicating that stimulation of glycogenolysis predominates in the periportal area.
  • The increases in perfusion pressure were more pronounced when the periportal area was supplied with NAD+ suggesting that the vasoconstrictive elements responding to NAD+ predominate in this region.
  • The response to extracellular NAD+ is thus unequally distributed in the liver.
  • As a paracrine agent, NAD+ is likely to be released locally.
  • [MeSH-major] Glucose / secretion. Liver / metabolism. Liver Glycogen / metabolism. NAD / metabolism

  • Hazardous Substances Data Bank. GLUCOSE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 John Wiley & Sons, Ltd.
  • (PMID = 15920702.001).
  • [ISSN] 0263-6484
  • [Journal-full-title] Cell biochemistry and function
  • [ISO-abbreviation] Cell Biochem. Funct.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Liver Glycogen; 0U46U6E8UK / NAD; IY9XDZ35W2 / Glucose
  •  go-up   go-down


62. Hoff KG, Avalos JL, Sens K, Wolberger C: Insights into the sirtuin mechanism from ternary complexes containing NAD+ and acetylated peptide. Structure; 2006 Aug;14(8):1231-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insights into the sirtuin mechanism from ternary complexes containing NAD+ and acetylated peptide.
  • Sirtuin proteins comprise a unique class of NAD+-dependent protein deacetylases.
  • Although several structures of sirtuins have been determined, the mechanism by which NAD+ cleavage occurs has remained unclear.
  • We report the structures of ternary complexes containing NAD+ and acetylated peptide bound to the bacterial sirtuin Sir2Tm and to a catalytic mutant (Sir2Tm(H116Y)).
  • NAD+ in these structures binds in a conformation different from that seen in previous structures, exposing the alpha face of the nicotinamide ribose to the carbonyl oxygen of the acetyl lysine substrate.
  • The NAD+ conformation is identical in both structures, suggesting that proper coenzyme orientation is not dependent on contacts with the catalytic histidine.
  • Taken together, these structures suggest a mechanism for nicotinamide cleavage in which an invariant phenylalanine plays a central role in promoting formation of the O-alkylamidate reaction intermediate and preventing nicotinamide exchange.
  • [MeSH-minor] Crystallization. Crystallography, X-Ray. NAD / chemistry. NAD / metabolism. O-Acetyl-ADP-Ribose / chemistry. O-Acetyl-ADP-Ribose / metabolism. Peptides / chemistry. Peptides / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16905097.001).
  • [ISSN] 0969-2126
  • [Journal-full-title] Structure (London, England : 1993)
  • [ISO-abbreviation] Structure
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2H4F/ 2H4H/ 2H4J/ 2H59
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-O-acetyl-ADP-ribose; 0 / Multiprotein Complexes; 0 / O-Acetyl-ADP-Ribose; 0 / Peptides; 0U46U6E8UK / NAD; EC 3.5.1.- / Sirtuins
  •  go-up   go-down


63. Tanno M, Sakamoto J, Miura T, Shimamoto K, Horio Y: Nucleocytoplasmic shuttling of the NAD+-dependent histone deacetylase SIRT1. J Biol Chem; 2007 Mar 2;282(9):6823-32
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nucleocytoplasmic shuttling of the NAD+-dependent histone deacetylase SIRT1.
  • Sir2 (silent information regulator 2) is an NAD(+)-dependent histone deacetylase that contributes to longevity in yeast.


64. Liu Q, Kriksunov IA, Jiang H, Graeff R, Lin H, Lee HC, Hao Q: Covalent and noncovalent intermediates of an NAD utilizing enzyme, human CD38. Chem Biol; 2008 Oct 20;15(10):1068-78
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Covalent and noncovalent intermediates of an NAD utilizing enzyme, human CD38.
  • Enzymatic utilization of nicotinamide adenine dinucleotide (NAD) has increasingly been shown to have fundamental roles in gene regulation, signal transduction, and protein modification.
  • Many of the processes require the cleavage of the nicotinamide moiety from the substrate and the formation of a reactive intermediate.
  • Using X-ray crystallography, we show that human CD38, an NAD-utilizing enzyme, is capable of catalyzing the cleavage reactions through both covalent and noncovalent intermediates, depending on the substrate used.
  • Our structural results favor the proposal of a noncovalent intermediate during normal enzymatic utilization of NAD by human CD38 and provide structural insights into the design of covalent and noncovalent inhibitors targeting NAD-utilization pathways.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem J. 2000 Jul 1;349(Pt 1):203-10 [10861229.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):649-55 [11001947.001]
  • [Cites] Nat Med. 2001 Nov;7(11):1209-16 [11689885.001]
  • [Cites] Biochemistry. 2002 Jul 2;41(26):8455-63 [12081495.001]
  • [Cites] FASEB J. 2003 Mar;17(3):369-75 [12631576.001]
  • [Cites] J Vet Med Sci. 2003 Dec;65(12):1325-30 [14709821.001]
  • [Cites] Immunity. 2004 Mar;20(3):279-91 [15030772.001]
  • [Cites] J Mol Biol. 2004 Apr 16;338(1):1-6 [15050818.001]
  • [Cites] Curr Med Chem. 2004 Apr;11(7):807-26 [15078167.001]
  • [Cites] Curr Med Chem. 2004 Apr;11(7):857-72 [15078170.001]
  • [Cites] Curr Mol Med. 2004 May;4(3):227-37 [15101681.001]
  • [Cites] Curr Mol Med. 2004 May;4(3):249-61 [15101683.001]
  • [Cites] Annu Rev Biochem. 2004;73:417-35 [15189148.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2004 Aug;60(Pt 8):1355-63 [15272157.001]
  • [Cites] J Biol Chem. 1978 Jul 25;253(14):5186-92 [209029.001]
  • [Cites] J Biol Chem. 1989 Jan 25;264(3):1608-15 [2912976.001]
  • [Cites] Acta Crystallogr A. 1991 Mar 1;47 ( Pt 2):110-9 [2025413.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Mar 15;191(2):639-45 [8461019.001]
  • [Cites] Science. 1993 Nov 12;262(5136):1056-9 [8235624.001]
  • [Cites] Mol Cell Biochem. 1994 Sep;138(1-2):229-35 [7898468.001]
  • [Cites] Mol Cell Biochem. 1994 Sep;138(1-2):245-51 [7898470.001]
  • [Cites] J Biol Chem. 1995 Dec 22;270(51):30327-33 [8530456.001]
  • [Cites] J Biol Chem. 1996 Sep 27;271(39):23967-72 [8798630.001]
  • [Cites] Biochemistry. 1998 Sep 22;37(38):13239-49 [9748331.001]
  • [Cites] J Biol Chem. 1999 Jan 22;274(4):1869-72 [9890936.001]
  • [Cites] Mol Cell Biochem. 1999 Mar;193(1-2):89-98 [10331643.001]
  • [Cites] Cell. 2005 Feb 25;120(4):497-512 [15734682.001]
  • [Cites] Science. 2005 Aug 12;309(5737):1093-6 [16099990.001]
  • [Cites] Structure. 2005 Sep;13(9):1331-9 [16154090.001]
  • [Cites] FEBS J. 2005 Sep;272(18):4590-7 [16156781.001]
  • [Cites] Biochemistry. 2006 Jan 10;45(1):272-82 [16388603.001]
  • [Cites] Microbiol Mol Biol Rev. 2006 Sep;70(3):789-829 [16959969.001]
  • [Cites] J Biol Chem. 2006 Oct 27;281(43):32861-9 [16951430.001]
  • [Cites] J Biol Chem. 2007 Feb 23;282(8):5853-61 [17182614.001]
  • [Cites] Nature. 2007 Mar 1;446(7131):41-5 [17287729.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):317-23 [17380198.001]
  • [Cites] Biochem J. 2007 May 15;404(1):1-13 [17447894.001]
  • [Cites] Chem Immunol. 2000;75:39-59 [10851778.001]
  • [Cites] J Biol Chem. 2000 Jul 14;275(28):21566-71 [10781610.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2001;41:317-45 [11264460.001]
  • (PMID = 18940667.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 3DZF/ 3DZG/ 3DZH/ 3DZI/ 3DZJ/ 3DZK
  • [Grant] United States / NCRR NIH HHS / RR / P41 RR001646-256438; United States / NIGMS NIH HHS / GM / GM061568-07; United States / NCRR NIH HHS / RR / RR01646; United States / NIGMS NIH HHS / GM / R01 GM061568-07; United States / NCRR NIH HHS / RR / RR001646-256438; United States / NCRR NIH HHS / RR / P41 RR001646; United States / NIGMS NIH HHS / GM / GM061568; United States / NIGMS NIH HHS / GM / DMR0225180; United States / NIGMS NIH HHS / GM / R01 GM061568
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycosides; 0U46U6E8UK / NAD; 1094-61-7 / Nicotinamide Mononucleotide; EC 3.2.2.5 / Antigens, CD38
  • [Other-IDs] NLM/ NIHMS75814; NLM/ PMC2607045
  •  go-up   go-down


65. Wozniacka A, Szajerski P, Adamus J, Gebicki J, Sysa-Jedrzejowska A: In search for new antipsoriatic agents: NAD topical composition. Skin Pharmacol Physiol; 2007;20(1):37-42
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In search for new antipsoriatic agents: NAD topical composition.
  • The aim of the study was to examine the effectiveness of the oxidized form of nicotinamide adenine dinucleotide (NAD(+)), adenosine precursor, in 37 patients suffering from psoriasis.
  • As NAD(+) is known to be relatively unstable, the second goal was to establish the proper conditions for the satisfactory stability of topical NAD(+) composition.
  • Topical treatment with 1 or 0.3% NAD(+) in Vaseline ointment administered twice daily was compared with overnight therapy with 0.1% anthralin applied for 12 h and placebo.
  • The enzymatic method was applied to determine the stability of NAD(+) in Vaseline ointment.
  • After a 4-week application, the reduction in erythema, infiltration and desquamation caused by 1 or 0.3% topical NAD(+) composition was similar to the reduction caused by 0.1% anthralin.
  • It was demonstrated that NAD(+) underwent a considerable decomposition at room temperature, while it was sufficiently stable at 5 degrees C; thus, for a longer use the agent should be stored at fridge temperature.
  • NAD(+) therapy combines good efficacy, cosmetic acceptability and convenient twice-daily application.
  • [MeSH-major] Dermatologic Agents / therapeutic use. NAD / therapeutic use. Psoriasis / drug therapy

  • MedlinePlus Health Information. consumer health - Psoriasis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17035720.001).
  • [ISSN] 1660-5527
  • [Journal-full-title] Skin pharmacology and physiology
  • [ISO-abbreviation] Skin Pharmacol Physiol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dermatologic Agents; 0 / Ointments; 0U46U6E8UK / NAD; U8CJK0JH5M / Anthralin
  •  go-up   go-down


66. Zhou H, Zhang Z, Yu P, Su L, Ohsaka T, Mao L: Noncovalent attachment of NAD+ cofactor onto carbon nanotubes for preparation of integrated dehydrogenase-based electrochemical biosensors. Langmuir; 2010 Apr 20;26(8):6028-32
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Noncovalent attachment of NAD+ cofactor onto carbon nanotubes for preparation of integrated dehydrogenase-based electrochemical biosensors.
  • This study describes a facile approach to the preparation of integrated dehydrogenase-based electrochemical biosensors through noncovalent attachment of an oxidized form of beta-nicotinamide adenine dinucleotide (NAD(+)) onto carbon nanotubes with the interaction between the adenine subunit in NAD(+) molecules and multiwalled carbon nanotubes (MWCNTs).
  • X-ray photoelectron spectroscopic and cyclic voltammetric results suggest that NAD(+) is noncovalently attached onto MWCNTs to form an NAD(+)/MWCNT composite that acts as the electronic transducer for the integrated dehydrogenase-based electrochemical biosensors.
  • With glucose dehydrogenase (GDH) as a model dehydrogenase-based recognition unit, electrochemical studies reveal that glucose is readily oxidized at the GDH/NAD(+)/MWCNT-modified electrode without addition of NAD(+) in the phosphate buffer.
  • The potential for the oxidation of glucose at the GDH/NAD(+)/MWCNT-modified electrode remains very close to that for NADH oxidation at the MWCNT-modified electrode, but it is more negative than those for the oxidation of glucose at the MWCNT-modified electrode and for NADH oxidation at a bare glassy carbon electrode.
  • These results demonstrate that NAD(+) molecules stably attached onto MWCNTs efficiently act as the cofactor for the dehydrogenases.
  • MWCNTs employed here not only serve as the electronic transducer and the support to confine NAD(+) cofactor onto the electrode surface, but also act as the electrocatalyst for NADH oxidation in the dehydrogenase-based electrochemical biosensors.
  • At the GDH/NAD(+)/MWCNT-based glucose biosensor, the current is linear with the concentration of glucose being within a concentration range from 10 to 300 microM with a limit of detection down to 4.81 microM (S/N = 3).
  • [MeSH-major] Biosensing Techniques / methods. Electrochemistry / methods. Glucose 1-Dehydrogenase / chemistry. Glucose 1-Dehydrogenase / metabolism. NAD / chemistry. Nanotubes, Carbon / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20121055.001).
  • [ISSN] 1520-5827
  • [Journal-full-title] Langmuir : the ACS journal of surfaces and colloids
  • [ISO-abbreviation] Langmuir
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nanotubes, Carbon; 0U46U6E8UK / NAD; EC 1.1.1.47 / Glucose 1-Dehydrogenase
  •  go-up   go-down


67. Grose JH, Bergthorsson U, Roth JR: Regulation of NAD synthesis by the trifunctional NadR protein of Salmonella enterica. J Bacteriol; 2005 Apr;187(8):2774-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of NAD synthesis by the trifunctional NadR protein of Salmonella enterica.
  • The N-terminal domain represses transcription of genes for NAD synthesis and salvage.
  • The C-terminal domain has nicotinamide ribose kinase (NmR-K; EC 2.7.1.22) activity, which is essential for assimilation of NmR, converting it internally to nicotinamide mononucleotide (NMN).
  • The central domain has a weak adenylyltransferase (NMN-AT; EC 2.7.7.1) activity that converts NMN directly to NAD but is physiologically irrelevant.
  • This central domain mediates regulatory effects of NAD on all NadR activities.
  • NAD allows NadR to bind DNA in the presence of ATP and causes repression in vivo.
  • The mutant protein shows full NmR kinase activity that is 10-fold more sensitive to NAD inhibition than the wild type.
  • It is proposed that NAD and the superrepressor mutation exert their effects by preventing ATP from binding to the central domain.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mol Biol. 1990 Oct 5;215(3):403-10 [2231712.001]
  • [Cites] J Bacteriol. 1989 Aug;171(8):4402-9 [2546921.001]
  • [Cites] J Bacteriol. 1991 Feb;173(3):1311-20 [1991724.001]
  • [Cites] FEMS Microbiol Lett. 1993 Sep 1;112(2):179-83 [8405960.001]
  • [Cites] Nucleic Acids Res. 1994 Nov 11;22(22):4673-80 [7984417.001]
  • [Cites] Anal Biochem. 1995 Jun 10;228(1):64-8 [8572289.001]
  • [Cites] Mol Gen Genet. 1996 Sep 25;252(4):456-64 [8879247.001]
  • [Cites] Adv Exp Med Biol. 1997;419:381-8 [9193680.001]
  • [Cites] J Bacteriol. 1999 Jan;181(2):648-55 [9882682.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1999;73:135-82, xi [10218108.001]
  • [Cites] J Bacteriol. 1999 Sep;181(17):5509-11 [10464228.001]
  • [Cites] J Biol Chem. 1956 Jan;218(1):97-106 [13278318.001]
  • [Cites] J Biol Chem. 2002 Sep 6;277(36):33291-9 [12068016.001]
  • [Cites] J Mol Microbiol Biotechnol. 1999 Aug;1(1):127-8 [10941793.001]
  • [Cites] J Bacteriol. 2001 Jul;183(13):3974-81 [11395461.001]
  • [Cites] Eur J Biochem. 2001 Aug;268(15):4359-65 [11488932.001]
  • [Cites] J Bacteriol. 2002 Mar;184(5):1474-80 [11844783.001]
  • [Cites] J Bacteriol. 2002 Dec;184(24):6906-17 [12446641.001]
  • [Cites] Science. 2002 Dec 20;298(5602):2390-2 [12493915.001]
  • [Cites] Microbiology. 2003 Apr;149(Pt 4):983-90 [12686640.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1968;33:21-6 [4306814.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1968;33:27-34 [4306816.001]
  • [Cites] J Biol Chem. 1971 Feb 25;246(4):1107-16 [5543676.001]
  • [Cites] Anal Biochem. 1972 Mar;46(1):181-6 [4336011.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968.001]
  • [Cites] J Biol Chem. 1979 Jul 25;254(14):6270-2 [221495.001]
  • [Cites] CRC Crit Rev Biochem. 1985;17(4):313-451 [3157549.001]
  • [Cites] J Gen Microbiol. 1985 Jun;131(6):1313-22 [3900274.001]
  • [Cites] J Bacteriol. 1987 Jan;169(1):184-8 [3025169.001]
  • [Cites] Mol Gen Genet. 1987 Jun;208(1-2):279-87 [3039308.001]
  • [Cites] J Bacteriol. 1988 Jan;170(1):117-25 [3275606.001]
  • [Cites] Science. 1988 Apr 29;240(4852):640-2 [2834821.001]
  • [Cites] Science. 1988 Jun 3;240(4857):1302-9 [3287616.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4799-803 [2838846.001]
  • [Cites] J Bacteriol. 1989 Apr;171(4):2173-80 [2649488.001]
  • [Cites] J Bacteriol. 1991 Feb;173(3):1302-10 [1991723.001]
  • (PMID = 15805524.001).
  • [ISSN] 0021-9193
  • [Journal-full-title] Journal of bacteriology
  • [ISO-abbreviation] J. Bacteriol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM23408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / DNA, Bacterial; 0 / NadR protein, bacteria; 0 / Repressor Proteins; 0U46U6E8UK / NAD
  • [Other-IDs] NLM/ PMC1070365
  •  go-up   go-down


68. Ménétrey J, Flatau G, Boquet P, Ménez A, Stura EA: Structural basis for the NAD-hydrolysis mechanism and the ARTT-loop plasticity of C3 exoenzymes. Protein Sci; 2008 May;17(5):878-86
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural basis for the NAD-hydrolysis mechanism and the ARTT-loop plasticity of C3 exoenzymes.
  • This modification process goes through three sequential steps involving NAD-hydrolysis, Rho recognition, and binding, leading to Rho ADP-ribosylation.
  • Supporting the critical role of the ARTT loop, we have shown previously that it adopts a distinct conformation upon NAD binding.
  • Here, we present seven wild-type and ARTT loop-mutant structures of C3 exoenzyme of Clostridium botulinum free and bound to its true substrate, NAD, and to its NAD-hydrolysis product, nicotinamide.
  • [MeSH-major] ADP Ribose Transferases / chemistry. Botulinum Toxins / chemistry. NAD / chemistry

  • Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .
  • Hazardous Substances Data Bank. ASPARAGINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Biophys Res Commun. 1991 Jan 31;174(2):459-64 [1993048.001]
  • [Cites] J Biol Chem. 1989 May 25;264(15):8602-5 [2498316.001]
  • [Cites] J Biol Chem. 1992 May 25;267(15):10274-80 [1587816.001]
  • [Cites] Biochemistry. 1995 Jan 10;34(1):334-40 [7819216.001]
  • [Cites] FEBS Lett. 1995 Sep 4;371(2):105-9 [7672106.001]
  • [Cites] Biochimie. 1995;77(5):326-32 [8527485.001]
  • [Cites] Biochemistry. 1996 Jan 9;35(1):282-9 [8555186.001]
  • [Cites] Biochemistry. 1998 Apr 14;37(15):5296-304 [9548761.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1999 Apr;55(Pt 4):938-40 [10089341.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 2004;152:1-22 [15372308.001]
  • [Cites] J Mol Biol. 2001 Jan 5;305(1):95-107 [11114250.001]
  • [Cites] J Biol Chem. 2001 Mar 23;276(12):9537-42 [11124969.001]
  • [Cites] Infect Immun. 2001 Dec;69(12):7760-71 [11705958.001]
  • [Cites] Biochemistry. 2002 Feb 5;41(5):1539-44 [11814347.001]
  • [Cites] Int J Med Microbiol. 2002 Feb;291(6-7):523-9 [11890553.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):14771-6 [11847234.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):30950-7 [12029083.001]
  • [Cites] Nature. 2002 Dec 12;420(6916):629-35 [12478284.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Feb 28;302(1):127-32 [12593858.001]
  • [Cites] J Biol Chem. 2003 Aug 1;278(31):28523-7 [12750364.001]
  • [Cites] Biochemistry. 2003 Aug 19;42(32):9694-702 [12911311.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45924-30 [12933793.001]
  • [Cites] Mol Cell Biol. 1988 Jan;8(1):418-26 [3122025.001]
  • [Cites] Biochem J. 1987 Oct 15;247(2):363-8 [3122724.001]
  • [Cites] Eur J Biochem. 1988 Mar 1;172(2):445-50 [3127209.001]
  • [Cites] J Biol Chem. 1991 Oct 15;266(29):19312-9 [1918048.001]
  • (PMID = 18369192.001).
  • [ISSN] 1469-896X
  • [Journal-full-title] Protein science : a publication of the Protein Society
  • [ISO-abbreviation] Protein Sci.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2C89/ 2C8A/ 2C8B/ 2C8C/ 2C8D/ 2C8E/ 2C8F
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 3KX376GY7L / Glutamic Acid; 7006-34-0 / Asparagine; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.- / exoenzyme C3, Clostridium botulinum; EC 3.4.24.69 / Botulinum Toxins
  • [Other-IDs] NLM/ PMC2327275
  •  go-up   go-down


69. Franchetti P, Petrelli R, Cappellacci L, Pasqualini M, Vita P, Sorci L, Mazzola F, Raffaelli N, Magni G: Synthesis and biological evaluation of NAD analogs as human pyridine nucleotide adenylyltransferase inhibitors. Nucleosides Nucleotides Nucleic Acids; 2005;24(5-7):477-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis and biological evaluation of NAD analogs as human pyridine nucleotide adenylyltransferase inhibitors.
  • NAD analogs modified at the ribose adenylyl moiety, named N-2'-MeAD and Na-2'-MeAD, were synthesized as ligands of pyridine nucleotide (NMN/NaMN) adenylyltransferase (NMNAT).
  • [MeSH-major] Enzyme Inhibitors / chemical synthesis. NAD / chemical synthesis. Nicotinamide-Nucleotide Adenylyltransferase / antagonists & inhibitors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16247974.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Ligands; 0U46U6E8UK / NAD; EC 2.7.7.1 / Nicotinamide-Nucleotide Adenylyltransferase
  •  go-up   go-down


70. Imai S: Toward productive aging: SIRT1, systemic NAD biosynthesis, and the NAD world. Cornea; 2010 Nov;29 Suppl 1:S7-12
MedlinePlus Health Information. consumer health - Seniors' Health.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Toward productive aging: SIRT1, systemic NAD biosynthesis, and the NAD world.
  • To achieve this goal, we have been studying mechanisms of mammalian aging and longevity, focusing on the physiological importance of the mammalian nicotinamide adenine dinucleotide (NAD)--dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase for the regulation of metabolism and aging.
  • Through these studies, we have recently proposed a comprehensive concept of a novel systemic regulatory network for metabolism and aging, named "NAD World."
  • This new concept of NAD World also conveys ideas of functional hierarchy and frailty for the induction of aging in mammals.
  • Details of the NAD World and its implications to age-associated metabolic diseases such as type 2 diabetes will be discussed.
  • [MeSH-major] Aging / physiology. NAD / biosynthesis. Sirtuin 1 / physiology
  • [MeSH-minor] Cytokines / metabolism. Energy Metabolism. Humans. Nicotinamide Phosphoribosyltransferase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20935547.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG024150
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human; EC 3.5.1.- / SIRT1 protein, human; EC 3.5.1.- / Sirtuin 1
  •  go-up   go-down


71. Sorci L, Blaby I, De Ingeniis J, Gerdes S, Raffaelli N, de Crécy Lagard V, Osterman A: Genomics-driven reconstruction of acinetobacter NAD metabolism: insights for antibacterial target selection. J Biol Chem; 2010 Dec 10;285(50):39490-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomics-driven reconstruction of acinetobacter NAD metabolism: insights for antibacterial target selection.
  • Enzymes involved in the last steps of NAD biogenesis, nicotinate mononucleotide adenylyltransferase (NadD) and NAD synthetase (NadE), are conserved and essential in most bacterial species and are established targets for antibacterial drug development.
  • Our genomics-based reconstruction of NAD metabolism in the emerging pathogen Acinetobacter baumannii revealed unique features suggesting an alternative targeting strategy.
  • We combined bioinformatics with genetic and biochemical techniques to elucidate this and other important features of Acinetobacter NAD metabolism using a model (nonpathogenic) strain Acinetobacter baylyi sp. ADP1.
  • Thus, a comparative kinetic characterization of PncA, PncB, and NadV enzymes allowed us to suggest distinct physiological roles for the two alternative, deamidating and nondeamidating, routes of nicotinamide salvage/recycling.
  • The role of the NiaP transporter in both nicotinate and nicotinamide salvage was confirmed.
  • The NadM enzyme was shown to possess dual substrate specificity toward both nicotinate and nicotinamide mononucleotide substrates, which is consistent with its essential role in all three routes of NAD biogenesis, de novo synthesis as well as the two salvage pathways.
  • In contrast, nadE, encoding a glutamine-dependent NAD synthetase, proved to be dispensable when the nondeamidating salvage pathway functioned as the only route of NAD biogenesis.
  • [MeSH-major] Acinetobacter baumannii / metabolism. Anti-Bacterial Agents / pharmacology. Genomics. NAD / chemistry
  • [MeSH-minor] Cloning, Molecular. Computational Biology / methods. Escherichia coli / metabolism. Humans. Kinetics. Models, Chemical. Models, Genetic. Mutation. Nicotinamide-Nucleotide Adenylyltransferase / metabolism. Phenotype. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Antibiotics.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 2004;32(19):5766-79 [15514110.001]
  • [Cites] Chem Biol. 2009 Aug 28;16(8):849-61 [19716475.001]
  • [Cites] Biochemistry. 1994 Nov 22;33(46):13662-7 [7947774.001]
  • [Cites] FEBS Lett. 1994 Dec 5;355(3):233-6 [7988679.001]
  • [Cites] J Bacteriol. 1997 Dec;179(24):7718-23 [9401030.001]
  • [Cites] Biochemistry. 1998 Mar 24;37(12):4189-99 [9521741.001]
  • [Cites] Microbiol Mol Biol Rev. 2009 Sep;73(3):529-41, Table of Contents [19721089.001]
  • [Cites] Curr Opin Microbiol. 2009 Oct;12(5):568-76 [19709925.001]
  • [Cites] Angew Chem Int Ed Engl. 2009;48(48):9176-9 [19859929.001]
  • [Cites] Nucleic Acids Res. 2010 Jan;38(Database issue):D111-8 [19884135.001]
  • [Cites] Nucleic Acids Res. 2010 Jan;38(Database issue):D396-400 [19906701.001]
  • [Cites] Mol Microbiol. 2010 Apr;76(2):365-77 [20199601.001]
  • [Cites] J Comb Chem. 2009 Jul-Aug;11(4):617-25 [19408950.001]
  • [Cites] J Med Chem. 2010 Jul 22;53(14):5229-39 [20578699.001]
  • [Cites] Appl Environ Microbiol. 2010 Aug;76(16):5488-95 [20601509.001]
  • [Cites] Mol Syst Biol. 2010 Sep 7;6:408 [20823846.001]
  • [Cites] J Bacteriol. 1998 Nov;180(22):5809-14 [9811635.001]
  • [Cites] FEBS Lett. 1999 Feb 12;444(2-3):222-6 [10050763.001]
  • [Cites] Nucleic Acids Res. 2005;33(17):5691-702 [16214803.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36334-41 [16118205.001]
  • [Cites] Cell Mol Life Sci. 2006 Jan;63(2):123-43 [16378245.001]
  • [Cites] J Bacteriol. 2006 Apr;188(8):3012-23 [16585762.001]
  • [Cites] Nat Struct Mol Biol. 2006 Jul;13(7):582-8 [16783377.001]
  • [Cites] J Bacteriol. 2006 Oct;188(19):6719-27 [16980474.001]
  • [Cites] Prog Drug Res. 2007;64:131, 133-70 [17195474.001]
  • [Cites] Biochemistry. 2007 Apr 24;46(16):4912-22 [17402747.001]
  • [Cites] J Bacteriol. 2001 Jan;183(1):292-300 [11114929.001]
  • [Cites] Microbiology. 2002 Jan;148(Pt 1):325-32 [11782525.001]
  • [Cites] Proteins. 2002 Jul 1;48(1):1-14 [12012333.001]
  • [Cites] J Bacteriol. 2002 Aug;184(16):4555-72 [12142426.001]
  • [Cites] Eur J Immunol. 2002 Nov;32(11):3225-34 [12555668.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33049-55 [12771147.001]
  • [Cites] Appl Environ Microbiol. 2003 Oct;69(10):5892-7 [14532041.001]
  • [Cites] J Antimicrob Chemother. 2007 Jun;59(6):1210-5 [17324960.001]
  • [Cites] J Med Chem. 2007 May 31;50(11):2612-21 [17489580.001]
  • [Cites] Nat Rev Microbiol. 2007 Dec;5(12):939-51 [18007677.001]
  • [Cites] Structure. 2008 Feb;16(2):196-209 [18275811.001]
  • [Cites] Mol Syst Biol. 2008;4:174 [18319726.001]
  • [Cites] Nucleic Acids Res. 2008 Apr;36(6):2047-59 [18276643.001]
  • [Cites] Nucleic Acids Res. 2008 Apr;36(6):2032-46 [18276644.001]
  • [Cites] J Biol Chem. 2008 Jul 11;283(28):19329-41 [18490451.001]
  • [Cites] Biochemistry. 2008 Oct 21;47(42):11086-96 [18823127.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3083-8 [19204287.001]
  • [Cites] Bioorg Med Chem Lett. 2009 Apr 1;19(7):2001-5 [19249205.001]
  • [Cites] Nat Struct Mol Biol. 2009 Apr;16(4):421-9 [19270703.001]
  • [Cites] Curr Med Chem. 2009;16(11):1372-90 [19355893.001]
  • [Cites] Nucleic Acids Res. 2004;32(19):5780-90 [15514111.001]
  • (PMID = 20926389.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI066244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0U46U6E8UK / NAD; EC 2.7.7.1 / Nicotinamide-Nucleotide Adenylyltransferase; EC 2.7.7.18 / nicotinic acid mononucleotide adenylyltransferase
  • [Other-IDs] NLM/ PMC2998121
  •  go-up   go-down


72. Díaz S, Pérez-Pomares F, Pire C, Ferrer J, Bonete MJ: Gene cloning, heterologous overexpression and optimized refolding of the NAD-glutamate dehydrogenase from Haloferax mediterranei. Extremophiles; 2006 Apr;10(2):105-15
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene cloning, heterologous overexpression and optimized refolding of the NAD-glutamate dehydrogenase from Haloferax mediterranei.
  • The NAD-dependent glutamate dehydrogenase (GDH) gene from the halophilic archaeon Haloferax mediterranei has been cloned.
  • The analysis of the nucleotide sequence revealed an open reading frame of 1323 bp that encodes a NAD-GDH.
  • The expression of this gene in Escherichia coli, the refolding and further characterization, yielded a fully active NAD-GDH with the same features than those found for the wild-type enzyme.
  • This halophilic NAD-GDH showed a highly dependence on salts for both stability and activity, being essential for the refolding of the recombinant enzyme.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16200391.001).
  • [ISSN] 1431-0651
  • [Journal-full-title] Extremophiles : life under extreme conditions
  • [ISO-abbreviation] Extremophiles
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Archaeal Proteins; 0 / Recombinant Proteins; EC 1.4.1.2 / Glutamate Dehydrogenase
  •  go-up   go-down


73. Christensen KE, Mirza IA, Berghuis AM, Mackenzie RE: Magnesium and phosphate ions enable NAD binding to methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase. J Biol Chem; 2005 Oct 7;280(40):34316-23
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Magnesium and phosphate ions enable NAD binding to methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase.
  • The mitochondrial NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (NMDMC) is believed to have evolved from a trifunctional NADP-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase-synthetase.
  • The model supports the hypothesis that the absolutely required Pi can bind in close proximity to the 2'-hydroxyl of NAD through interactions with Arg166 and Arg198.
  • Mutants of Asp133 suggest that the magnesium ion interacts with both Pi and the aspartate side chain and plays a role in positioning Pi and NAD.
  • NMDMC uses Pi and magnesium to adapt an NADP binding site for NAD binding.
  • [MeSH-major] Aminohydrolases / chemistry. Aminohydrolases / metabolism. Magnesium / physiology. Methylenetetrahydrofolate Dehydrogenase (NADP) / chemistry. Methylenetetrahydrofolate Dehydrogenase (NADP) / metabolism. Multienzyme Complexes / chemistry. Multienzyme Complexes / metabolism. NAD / metabolism. Phosphates / physiology

  • Hazardous Substances Data Bank. (L)-ARGININE .
  • Hazardous Substances Data Bank. MAGNESIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16100107.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 1ZN4
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coenzymes; 0 / Ions; 0 / Multienzyme Complexes; 0 / Phosphates; 0 / methylene tetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase; 0U46U6E8UK / NAD; 94ZLA3W45F / Arginine; EC 1.5.1.5 / Methylenetetrahydrofolate Dehydrogenase (NADP); EC 3.5.4.- / Aminohydrolases; I38ZP9992A / Magnesium
  •  go-up   go-down


74. Micheli V, Jacomelli G, Di Marcello F, Notarantonio L, Sestini S, Cerboni B, Bertelli M, Pompucci G, Jinnah HA: NAD metabolism in HPRT-deficient mice. Metab Brain Dis; 2009 Jun;24(2):311-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD metabolism in HPRT-deficient mice.
  • The activity of hypoxanthine-guanine phosphoribosyltransferase (HPRT) is virtually absent in Lesch-Nyhan disease (LND), an X-linked genetic disorder characterized by uric acid accumulation and neurodevelopmental dysfunction.
  • Prior studies of cells from affected patients have shown abnormalities of NAD metabolism.
  • In the current studies, NAD metabolism was evaluated in HPRT gene knock-out mice.
  • NAD content and the activities of the enzymes required for synthesis and breakdown of this coenzyme were investigated in blood, brain and liver of HPRT(-) and control mice.
  • NAD concentration and enzyme activities were found to be significantly increased in liver, but not in brain or blood of the HPRT(-) mice.
  • These results demonstrate that changes in NAD metabolism occur in response to HPRT deficiency depending on both species and tissue type.
  • [MeSH-major] Hypoxanthine Phosphoribosyltransferase / metabolism. Lesch-Nyhan Syndrome / enzymology. Liver / metabolism. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19319672.001).
  • [ISSN] 1573-7365
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD053312
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Purines; 0 / Pyridines; 0U46U6E8UK / NAD; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
  • [Other-IDs] NLM/ NIHMS785541; NLM/ PMC4876432
  •  go-up   go-down


75. Houtkooper RH, Cantó C, Wanders RJ, Auwerx J: The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. Endocr Rev; 2010 Apr;31(2):194-223
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways.
  • A century after the identification of a coenzymatic activity for NAD(+), NAD(+) metabolism has come into the spotlight again due to the potential therapeutic relevance of a set of enzymes whose activity is tightly regulated by the balance between the oxidized and reduced forms of this metabolite.
  • In fact, the actions of NAD(+) have been extended from being an oxidoreductase cofactor for single enzymatic activities to acting as substrate for a wide range of proteins.
  • These include NAD(+)-dependent protein deacetylases, poly(ADP-ribose) polymerases, and transcription factors that affect a large array of cellular functions.
  • Through these effects, NAD(+) provides a direct link between the cellular redox status and the control of signaling and transcriptional events.
  • Of particular interest within the metabolic/endocrine arena are the recent results, which indicate that the regulation of these NAD(+)-dependent pathways may have a major contribution to oxidative metabolism and life span extension.
  • 1) the pathways that control NAD(+) production and cycling, as well as its cellular compartmentalization;.
  • 2) the signaling and transcriptional pathways controlled by NAD(+); and 3) novel data that show how modulation of NAD(+)-producing and -consuming pathways have a major physiological impact and hold promise for the prevention and treatment of metabolic disease.
  • [MeSH-major] Metabolic Diseases / metabolism. NAD / metabolism

  • MedlinePlus Health Information. consumer health - Metabolic Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochimie. 1995;77(5):394-8 [8527495.001]
  • [Cites] Nat Med. 2009 Feb;15(2):151-8 [19182797.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6823-32 [17197703.001]
  • [Cites] Nature. 2003 Sep 11;425(6954):191-6 [12939617.001]
  • [Cites] Biochem J. 2007 May 15;404(1):1-13 [17447894.001]
  • [Cites] J Nutr. 1995 Jun;125(6):1455-61 [7782898.001]
  • [Cites] Mol Cell. 2003 Jul;12(1):51-62 [12887892.001]
  • [Cites] Curr Top Cell Regul. 1982;21:175-87 [6291854.001]
  • [Cites] Cell Biochem Funct. 2002 Dec;20(4):309-22 [12415565.001]
  • [Cites] Eur J Biochem. 1979 Nov 1;101(1):135-42 [228934.001]
  • [Cites] J Biol Chem. 1958 Aug;233(2):488-92 [13563526.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2570-80 [10521401.001]
  • [Cites] Structure. 2005 Sep;13(9):1385-96 [16154095.001]
  • [Cites] J Biol Chem. 1982 Nov 10;257(21):12872-7 [6813330.001]
  • [Cites] Cell. 2006 Jan 27;124(2):315-29 [16439206.001]
  • [Cites] Biochem Pharmacol. 1977 Dec 1;26(23):2251-8 [73376.001]
  • [Cites] J Biol Chem. 2008 Mar 28;283(13):8075-9 [18258590.001]
  • [Cites] Cell. 2006 Oct 20;127(2):397-408 [17055439.001]
  • [Cites] J Biol Chem. 2007 Aug 24;282(34):24574-82 [17604275.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17860-8 [10364231.001]
  • [Cites] Mol Cell Biol. 2003 May;23(9):3173-85 [12697818.001]
  • [Cites] Annu Rev Nutr. 2008;28:115-30 [18429699.001]
  • [Cites] J Biol Chem. 2004 Sep 17;279(38):40122-9 [15269219.001]
  • [Cites] J Cell Biol. 2002 Aug 19;158(4):647-57 [12186850.001]
  • [Cites] FEBS Lett. 2001 Mar 9;492(1-2):95-100 [11248244.001]
  • [Cites] Cell Metab. 2006 Jan;3(1):35-45 [16399503.001]
  • [Cites] J Pharmacol Exp Ther. 2008 Mar;324(3):883-93 [18165311.001]
  • [Cites] PLoS Biol. 2006 Feb;4(2):e31 [16366736.001]
  • [Cites] Curr Biol. 2003 Apr 15;13(8):669-73 [12699624.001]
  • [Cites] J Cell Physiol. 1976 Jun;88(2):207-17 [178671.001]
  • [Cites] Science. 2009 May 1;324(5927):651-4 [19299583.001]
  • [Cites] Nature. 2005 Mar 3;434(7029):113-8 [15744310.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1075-80 [16618798.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Aug;76(8):4084-6 [291064.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8122-35 [16923962.001]
  • [Cites] Science. 2004 Mar 26;303(5666):2011-5 [14976264.001]
  • [Cites] Nature. 2008 Mar 27;452(7186):492-6 [18337721.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):686-9 [15254550.001]
  • [Cites] FASEB J. 2007 Nov;21(13):3629-39 [17585054.001]
  • [Cites] Cell. 2008 Jul 25;134(2):329-40 [18662547.001]
  • [Cites] J Biol Chem. 2009 Jun 19;284(25):17110-9 [19416965.001]
  • [Cites] Science. 2006 Jun 23;312(5781):1798-802 [16794079.001]
  • [Cites] Cell. 2007 Sep 21;130(6):1095-107 [17889652.001]
  • [Cites] FASEB J. 1992 Aug;6(11):2977-89 [1322853.001]
  • [Cites] PLoS Med. 2007 Mar;4(3):e76 [17341128.001]
  • [Cites] Curr Med Chem. 2009;16(11):1372-90 [19355893.001]
  • [Cites] Biochem Biophys Res Commun. 2009 Jan 23;378(4):836-41 [19071085.001]
  • [Cites] Oncogene. 2007 Feb 15;26(7):945-57 [16909107.001]
  • [Cites] Nature. 2003 May 8;423(6936):181-5 [12736687.001]
  • [Cites] Nat Med. 2003 Mar;9(3):352-5 [12563315.001]
  • [Cites] J Biol Chem. 1972 Feb 10;247(3):778-83 [4333514.001]
  • [Cites] EMBO J. 1995 Jul 17;14(14):3480-6 [7628449.001]
  • [Cites] Anal Biochem. 2006 May 15;352(2):282-5 [16574057.001]
  • [Cites] Trends Biochem Sci. 2004 Mar;29(3):111-8 [15003268.001]
  • [Cites] Cell Metab. 2007 Nov;6(5):363-75 [17983582.001]
  • [Cites] Brain. 1992 Oct;115 ( Pt 5):1249-73 [1422788.001]
  • [Cites] Nature. 2007 Nov 29;450(7170):712-6 [18046409.001]
  • [Cites] J Biol Chem. 2007 Apr 13;282(15):10841-5 [17307730.001]
  • [Cites] Prog Neurobiol. 2007 Oct;83(3):174-91 [17822833.001]
  • [Cites] Cell Metab. 2008 Aug;8(2):157-68 [18599363.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Aug;4(8):641-9 [12923526.001]
  • [Cites] J Neurosci. 2003 Apr 1;23(7):2833-9 [12684470.001]
  • [Cites] Nature. 2000 Feb 17;403(6771):795-800 [10693811.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):123-8 [19132007.001]
  • [Cites] Cell. 2005 Feb 25;120(4):449-60 [15734678.001]
  • [Cites] Cell Metab. 2007 Jun;5(6):426-37 [17550778.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10230-5 [16790548.001]
  • [Cites] Nature. 2001 Sep 13;413(6852):131-8 [11557972.001]
  • [Cites] J Biol Chem. 1998 Nov 13;273(46):30069-72 [9804757.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21313-20 [15795229.001]
  • [Cites] Nature. 2006 Oct 19;443(7113):787-95 [17051205.001]
  • [Cites] Arch Biochem Biophys. 1955 Feb;54(2):558-9 [14350806.001]
  • [Cites] Biochem J. 1985 Sep 15;230(3):635-8 [3877502.001]
  • [Cites] J Biol Chem. 2006 Aug 4;281(31):21745-54 [16751189.001]
  • [Cites] Genomics. 1999 May 1;57(3):442-5 [10329013.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):23028-36 [11948190.001]
  • [Cites] Nature. 2002 Jul 18;418(6895):344-8 [12124627.001]
  • [Cites] J Microsc. 2008 Aug;231(2):299-316 [18778428.001]
  • [Cites] J Biochem. 1988 Jun;103(6):1054-9 [3139649.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):3059-64 [10077636.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 31;104(31):12861-6 [17646659.001]
  • [Cites] Protein Sci. 2009 Mar;18(3):514-25 [19241369.001]
  • [Cites] J Biol Chem. 1996 Aug 9;271(32):19140-5 [8702590.001]
  • [Cites] Int J Mol Med. 2005 Aug;16(2):237-43 [16012755.001]
  • [Cites] Cell Cycle. 2006 Apr;5(8):873-7 [16628003.001]
  • [Cites] FEMS Microbiol Rev. 2001 Jan;25(1):15-37 [11152939.001]
  • [Cites] Curr Biol. 2004 Feb 17;14(4):326-30 [14972684.001]
  • [Cites] Nat Rev Cancer. 2009 Jun;9(6):445-52 [19461669.001]
  • [Cites] Nat Neurosci. 2001 Dec;4(12):1199-206 [11770485.001]
  • [Cites] J Neurosci. 2007 Mar 7;27(10):2606-16 [17344398.001]
  • [Cites] Toxicol Appl Pharmacol. 1999 Jul 1;158(1):71-80 [10387934.001]
  • [Cites] Science. 2009 May 1;324(5927):654-7 [19286518.001]
  • [Cites] Nature. 2001 Mar 8;410(6825):227-30 [11242085.001]
  • [Cites] Diabetes. 2006 Jul;55(7):2153-6 [16804088.001]
  • [Cites] Ann Med. 2007;39(5):335-45 [17701476.001]
  • [Cites] Life Sci. 2008 Jan 16;82(3-4):205-9 [18078960.001]
  • [Cites] Cell. 2009 May 1;137(3):560-70 [19410549.001]
  • [Cites] Biochim Biophys Acta. 2000 Jan 3;1500(1):119-24 [10564724.001]
  • [Cites] J Biol Chem. 2007 Nov 16;282(46):33583-92 [17715127.001]
  • [Cites] Epilepsia. 1988 Sep-Oct;29(5):523-9 [3409840.001]
  • [Cites] Annu Rev Biochem. 2006;75:435-65 [16756498.001]
  • [Cites] Diabetologia. 2007 Dec;50(12):2476-85 [17922105.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):829-33 [17213307.001]
  • [Cites] Radiat Res. 1985 Jan;101(1):4-15 [3155867.001]
  • [Cites] J Neurosci. 2009 Apr 29;29(17):5525-35 [19403820.001]
  • [Cites] Mol Endocrinol. 2008 Apr;22(4):1006-14 [18187602.001]
  • [Cites] Trends Endocrinol Metab. 2009 Apr;20(3):130-8 [19109034.001]
  • [Cites] Br J Nutr. 1988 Mar;59(2):279-87 [2965917.001]
  • [Cites] Am J Pathol. 1998 Feb;152(2):611-9 [9466588.001]
  • [Cites] J Immunol. 2000 Apr 1;164(7):3596-9 [10725715.001]
  • [Cites] Cell. 2004 May 14;117(4):495-502 [15137942.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):835-40 [12359228.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13653-8 [12374852.001]
  • [Cites] FEBS J. 2005 Sep;272(18):4576-89 [16156780.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7436-42 [14612543.001]
  • [Cites] Cell. 2001 Oct 19;107(2):149-59 [11672523.001]
  • [Cites] Mol Aspects Med. 1983;6(2):101-97 [6371429.001]
  • [Cites] Genes Dev. 2006 May 15;20(10):1256-61 [16648462.001]
  • [Cites] FEBS Lett. 2003 Jun 5;544(1-3):74-8 [12782293.001]
  • [Cites] J Biol Chem. 2005 Apr 8;280(14):13560-7 [15653680.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9202-7 [12872005.001]
  • [Cites] J Biol Chem. 2009 Jul 24;284(30):20408-17 [19478080.001]
  • [Cites] AAPS J. 2006;8(4):E632-43 [17233528.001]
  • [Cites] Cell. 2008 Aug 8;134(3):405-15 [18674809.001]
  • [Cites] Cell Metab. 2005 Aug;2(2):105-17 [16098828.001]
  • [Cites] J Biol Chem. 2003 Mar 28;278(13):10914-21 [12547821.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50754-63 [15381699.001]
  • [Cites] Yeast. 2002 Feb;19(3):215-24 [11816029.001]
  • [Cites] J Biol Chem. 2005 Dec 30;280(52):43121-30 [16207712.001]
  • [Cites] Trends Endocrinol Metab. 2006 Jul;17(5):186-91 [16684606.001]
  • [Cites] Cell Metab. 2006 Jun;3(6):429-38 [16753578.001]
  • [Cites] Mol Cell Biol. 2007 Dec;27(24):8807-14 [17923681.001]
  • [Cites] J Biol Chem. 1948 Dec;176(3):1475 [18098602.001]
  • [Cites] Exp Cell Res. 1985 Oct;160(2):419-26 [2931297.001]
  • [Cites] Biochemistry. 1998 Sep 22;37(38):13239-49 [9748331.001]
  • [Cites] J Neurosci. 2006 Aug 16;26(33):8484-91 [16914673.001]
  • [Cites] Cell Mol Life Sci. 2004 Jan;61(1):19-34 [14704851.001]
  • [Cites] Gene. 2002 Feb 6;284(1-2):23-9 [11891043.001]
  • [Cites] Cell Death Differ. 2002 Oct;9(10):1069-77 [12232795.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10763-8 [8855254.001]
  • [Cites] Mol Biol Cell. 2005 Oct;16(10):4623-35 [16079181.001]
  • [Cites] Bioessays. 2003 Jul;25(7):683-90 [12815723.001]
  • [Cites] Lancet. 2004 Mar 20;363(9413):925-31 [15043959.001]
  • [Cites] Genes Dev. 2007 Apr 15;21(8):920-8 [17437997.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Sep;8(9):681-91 [17684529.001]
  • [Cites] J Biol Chem. 2003 Apr 11;278(15):13503-11 [12574164.001]
  • [Cites] Genes Dev. 2000 May 1;14(9):1021-6 [10809662.001]
  • [Cites] Eur J Pharmacol. 1981 Jul 10;72(4):411-2 [6268428.001]
  • [Cites] J Biol Chem. 2006 Mar 10;281(10):6120-3 [16436388.001]
  • [Cites] Biochim Biophys Acta. 1978 Nov 1;543(4):576-82 [214144.001]
  • [Cites] Mol Pharmacol. 2005 Jan;67(1):273-9 [15486050.001]
  • [Cites] Biochimie. 1995;77(6):403-7 [7578422.001]
  • [Cites] Biochim Biophys Acta. 2006 May-Jun;1757(5-6):721-6 [16730324.001]
  • [Cites] Immunology. 2002 Dec;107(4):452-60 [12460190.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Sep 26;309(3):558-66 [12963026.001]
  • [Cites] J Comp Neurol. 1990 May 1;295(1):71-82 [2341637.001]
  • [Cites] Genes Dev. 2008 Apr 1;22(7):931-44 [18381895.001]
  • [Cites] J Neurosci. 2008 May 7;28(19):4861-71 [18463239.001]
  • [Cites] Genomics. 2001 Apr 15;73(2):211-22 [11318611.001]
  • [Cites] Nat Rev Neurosci. 2005 Nov;6(11):889-98 [16224497.001]
  • [Cites] Annu Rev Biochem. 1960;29:669-708 [14409905.001]
  • [Cites] Biochemistry. 1990 Mar 13;29(10):2501-6 [2159322.001]
  • [Cites] Nat Med. 1999 Mar;5(3):314-9 [10086388.001]
  • [Cites] Cell. 2008 Jul 25;134(2):317-28 [18662546.001]
  • [Cites] Nature. 2009 Apr 23;458(7241):1056-60 [19262508.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Mar 3;341(1):67-72 [16412381.001]
  • [Cites] Microbes Infect. 2003 Jan;5(1):49-58 [12593973.001]
  • [Cites] Proc Natl Acad Sci U S A. 1978 Aug;75(8):3998-4000 [279015.001]
  • [Cites] J Physiol Pharmacol. 2008 Dec;59 Suppl 9:201-12 [19261981.001]
  • [Cites] Biochem Biophys Res Commun. 1963 Apr 2;11:39-43 [14019961.001]
  • [Cites] Br J Nutr. 1982 Jul;48(1):119-27 [6213259.001]
  • [Cites] Can J Vet Res. 2003 Jul;67(3):229-31 [12889731.001]
  • [Cites] Microbiol Mol Biol Rev. 2006 Sep;70(3):789-829 [16959969.001]
  • [Cites] Cell. 2006 Sep 8;126(5):941-54 [16959573.001]
  • [Cites] Science. 2004 Aug 13;305(5686):1010-3 [15310905.001]
  • [Cites] Genes Dev. 2008 Jul 1;22(13):1753-7 [18550784.001]
  • [Cites] Nature. 1981 Nov 19;294(5838):284-6 [6272129.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11377-82 [11027338.001]
  • [Cites] Science. 2005 Jan 21;307(5708):426-30 [15604363.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Apr;6(4):298-305 [15768047.001]
  • [Cites] Brain Res. 1985 Jun 17;336(2):207-14 [3159462.001]
  • [Cites] J Biol Chem. 1962 Mar;237:929-35 [14452547.001]
  • [Cites] Science. 2000 Sep 22;289(5487):2126-8 [11000115.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):406-12 [11027696.001]
  • [Cites] Cell Metab. 2007 Aug;6(2):105-14 [17681146.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982.001]
  • [Cites] Cell Death Differ. 2007 Jan;14(1):116-27 [16645633.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):334-41 [17380201.001]
  • [Cites] Exp Gerontol. 2003 Nov-Dec;38(11-12):1353-64 [14698816.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36334-41 [16118205.001]
  • [Cites] Cell Metab. 2008 Oct;8(4):333-41 [18840364.001]
  • [Cites] J Nutr. 2002 Jan;132(1):108-14 [11773516.001]
  • [Cites] Mol Cell. 2003 Feb;11(2):437-44 [12620231.001]
  • [Cites] Genes Dev. 2004 Jan 1;18(1):12-6 [14724176.001]
  • [Cites] J Biol Chem. 1993 Oct 25;268(30):22575-80 [8226768.001]
  • [Cites] J Biol Chem. 1965 Mar;240:1395-401 [14284754.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jul 14;345(4):1386-92 [16730329.001]
  • [Cites] J Biol Chem. 2008 Dec 12;283(50):34833-43 [18945671.001]
  • [Cites] Mol Endocrinol. 2006 Jul;20(7):1479-93 [16497729.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):317-23 [17380198.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):349-50 [15793589.001]
  • [Cites] Cell Metab. 2007 Oct;6(4):307-19 [17908559.001]
  • [Cites] Diabetologia. 2000 Nov;43(11):1337-45 [11126400.001]
  • [Cites] Nature. 2004 Jun 17;429(6993):771-6 [15175761.001]
  • [Cites] Nature. 2003 May 29;423(6939):550-5 [12754525.001]
  • [Cites] Biochem J. 2001 Sep 1;358(Pt 2):399-406 [11513738.001]
  • [Cites] Biochem J. 2008 Apr 15;411(2):e11-3 [18363549.001]
  • [Cites] EMBO J. 2007 Apr 4;26(7):1913-23 [17347648.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33056-9 [12777395.001]
  • [Cites] Dev Cell. 2008 May;14(5):661-73 [18477450.001]
  • [Cites] Am J Physiol. 1996 Oct;271(4 Pt 1):C1007-24 [8897805.001]
  • [Cites] Cell. 2006 Dec 15;127(6):1109-22 [17112576.001]
  • [Cites] Int J Dermatol. 2004 Jan;43(1):1-5 [14693013.001]
  • [Cites] J Biol Chem. 2007 Dec 28;282(52):37738-46 [17951580.001]
  • [Cites] Mol Cell Biol. 2008 Jan;28(2):814-24 [17991898.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Oct 13;349(1):353-9 [16935261.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):15998-6003 [15520384.001]
  • [Cites] Genomics. 2005 Feb;85(2):258-63 [15676284.001]
  • [Cites] Anal Biochem. 2009 Nov 1;394(1):101-9 [19615966.001]
  • [Cites] J Clin Invest. 2005 Jun;115(6):1627-35 [15902306.001]
  • [Cites] Biochem J. 1999 Sep 1;342 ( Pt 2):249-68 [10455009.001]
  • [Cites] Cell Metab. 2008 Nov;8(5):347-58 [19046567.001]
  • [Cites] Nature. 2006 Nov 16;444(7117):337-42 [17086191.001]
  • [Cites] J Cell Physiol. 1975 Dec;86 Suppl 2(3 Pt 2):641-51 [172520.001]
  • [Cites] Science. 2007 Oct 26;318(5850):565 [17962537.001]
  • [Cites] Biochem J. 1988 Aug 15;254(1):1-10 [3052428.001]
  • [Cites] Circ Res. 2008 Mar 28;102(6):703-10 [18239138.001]
  • [Cites] Nature. 2001 Sep 13;413(6852):179-83 [11557984.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14447-52 [18794531.001]
  • [Cites] Mol Cell Biol. 1994 Feb;14(2):1431-7 [8289818.001]
  • [Cites] Physiol Rev. 2008 Jul;88(3):841-86 [18626062.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10224-9 [16788062.001]
  • [Cites] Hum Mol Genet. 2007 Oct 1;16(19):2261-71 [17616514.001]
  • [Cites] Genomics. 1995 Sep 20;29(2):390-6 [8666386.001]
  • [Cites] J Clin Invest. 2004 May;113(9):1318-27 [15124023.001]
  • [Cites] Cell. 2004 Oct 1;119(1):121-35 [15454086.001]
  • [Cites] Cell Metab. 2005 Sep;2(3):153-63 [16154098.001]
  • [Cites] Curr Opin Cell Biol. 2008 Jun;20(3):303-9 [18468877.001]
  • [Cites] Arch Biochem Biophys. 1977 Nov;184(1):222-36 [21628.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Jun;40(6):1426-31 [8726014.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45099-107 [12297502.001]
  • [Cites] FEBS Lett. 2001 Mar 9;492(1-2):4-8 [11248227.001]
  • (PMID = 20007326.001).
  • [ISSN] 1945-7189
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Grant] International / European Research Council / / ERC/ 231138; United States / NIDDK NIH HHS / DK / P01 DK059820; United States / NIDDK NIH HHS / DK / DK59820
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; EC 1.- / Oxidoreductases
  • [Number-of-references] 248
  • [Other-IDs] NLM/ PMC2852209
  •  go-up   go-down


76. Mori S, Kawai S, Shi F, Mikami B, Murata K: Molecular conversion of NAD kinase to NADH kinase through single amino acid residue substitution. J Biol Chem; 2005 Jun 24;280(25):24104-12
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular conversion of NAD kinase to NADH kinase through single amino acid residue substitution.
  • NAD kinase phosphorylates NAD+ to form NADP+ and is strictly specific to NAD+, whereas NADH kinase phosphorylates both NAD+ and NADH, thereby showing relaxed substrate specificity.
  • Based on their primary and tertiary structures, the difference in the substrate specificities between NAD and NADH kinases was proposed to be caused by one aligned residue: Gly or polar amino acid (Gln or Thr) in five NADH kinases and a charged amino acid (Arg) in two NAD kinases.
  • The substitution of Arg with Gly in the two NAD kinases relaxed the substrate specificity (i.e. converted the NAD kinases to NADH kinases).
  • The substitution of Arg in one NAD kinase with polar amino acids also relaxed the substrate specificity, whereas substitution with charged and hydrophobic amino acids did not show a similar result.
  • In contrast, the substitution of Gly with Arg in one NADH kinase failed to convert it to NAD kinase.
  • These results suggest that a charged or hydrophobic amino acid residue in the position of interest is crucial for strict specificity of NAD kinases to NAD+, whereas Gly or polar amino acid residue is not the sole determinant for the relaxed substrate specificity of NADH kinases.
  • The significance of the conservation of the residue at the position in 207 NAD kinase homologues is also discussed.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15855156.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.23 / NAD kinase
  •  go-up   go-down


77. Lu SP, Lin SJ: Regulation of yeast sirtuins by NAD(+) metabolism and calorie restriction. Biochim Biophys Acta; 2010 Aug;1804(8):1567-75
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of yeast sirtuins by NAD(+) metabolism and calorie restriction.
  • The Sir2 family proteins (sirtuins) are evolutionally conserved NAD(+) (nicotinamide adenine dinucleotide)-dependent protein deacetylases and ADP-ribosylases, which have been shown to play important roles in the regulation of stress response, gene transcription, cellular metabolism and longevity.
  • Recent studies have also suggested that sirtuins are downstream targets of calorie restriction (CR), which mediate CR-induced beneficial effects including life span extension in an NAD(+)-dependent manner.
  • This review focuses on discussing advances in studies of sirtuins and NAD(+) metabolism in genetically tractable model system, the budding yeast Saccharomyces cerevisiae.
  • These studies have unraveled key metabolic longevity factors in the CR signaling and NAD(+) biosynthesis pathways, which may also contribute to the regulation of sirtuin activity.
  • Many components of the NAD(+) biosynthesis pathway and CR signaling pathway are conserved in yeast and higher eukaryotes including humans.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • [Cites] Trends Biochem Sci. 1998 Apr;23(4):131-4 [9584615.001]
  • [Cites] Exp Cell Res. 1998 Dec 15;245(2):379-88 [9851879.001]
  • [Cites] Cell. 2004 Feb 6;116(3):405-15 [15016375.001]
  • [Cites] Science. 2004 Mar 26;303(5666):2011-5 [14976264.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):686-9 [15254550.001]
  • [Cites] Mol Microbiol. 2004 Aug;53(4):1003-9 [15306006.001]
  • [Cites] J Biol Chem. 2004 Sep 17;279(38):40122-9 [15269219.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E296 [15328540.001]
  • [Cites] Mol Cell Biol. 1986 Feb;6(2):688-702 [3023863.001]
  • [Cites] Genetics. 1987 May;116(1):9-22 [3297920.001]
  • [Cites] Cell. 1990 Nov 16;63(4):751-62 [2225075.001]
  • [Cites] Mol Gen Genet. 1992 Jun;233(3):355-62 [1620093.001]
  • [Cites] Genes Dev. 1993 Apr;7(4):592-604 [8458576.001]
  • [Cites] Microbiol Rev. 1993 Jun;57(2):383-401 [8393130.001]
  • [Cites] J Biol Chem. 1994 Jul 15;269(28):18638-45 [8034612.001]
  • [Cites] Genes Dev. 1995 Dec 1;9(23):2888-902 [7498786.001]
  • [Cites] Nature. 1996 Sep 5;383(6595):92-6 [8779721.001]
  • [Cites] Genes Dev. 1997 Jan 1;11(1):83-93 [9000052.001]
  • [Cites] Aging Cell. 2007 Oct;6(5):649-62 [17711561.001]
  • [Cites] Cell Metab. 2007 Oct;6(4):280-93 [17908557.001]
  • [Cites] Science. 1999 Feb 12;283(5404):981-5 [9974390.001]
  • [Cites] Cell. 1999 Apr 16;97(2):245-56 [10219245.001]
  • [Cites] Mol Cell. 1999 Apr;3(4):447-55 [10230397.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2570-80 [10521401.001]
  • [Cites] J Biol Chem. 1958 Aug;233(2):488-92 [13563526.001]
  • [Cites] J Biol Chem. 1958 Aug;233(2):493-500 [13563527.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):15998-6003 [15520384.001]
  • [Cites] Nature. 2005 Mar 3;434(7029):113-8 [15744310.001]
  • [Cites] Cell. 2005 May 20;121(4):515-27 [15907466.001]
  • [Cites] J Bacteriol. 2005 Jul;187(13):4410-20 [15968050.001]
  • [Cites] J Bacteriol. 2005 Jul;187(13):4521-30 [15968063.001]
  • [Cites] Circ Res. 2005 Jul 8;97(1):25-34 [15947248.001]
  • [Cites] Gene. 2005 Jul 18;354:22-7 [15890475.001]
  • [Cites] Science. 2005 Sep 16;309(5742):1861-4 [16051752.001]
  • [Cites] Curr Opin Chem Biol. 2005 Oct;9(5):431-40 [16122969.001]
  • [Cites] Science. 2005 Oct 14;310(5746):314-7 [16224023.001]
  • [Cites] Cell. 2005 Nov 18;123(4):655-67 [16286010.001]
  • [Cites] Science. 2005 Nov 18;310(5751):1193-6 [16293764.001]
  • [Cites] Cell. 2007 May 4;129(3):473-84 [17482543.001]
  • [Cites] Mol Cell. 2004 Aug 13;15(3):409-21 [15304221.001]
  • [Cites] Nature. 2007 May 31;447(7144):545-9 [17538612.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10877-81 [17581878.001]
  • [Cites] Ageing Res Rev. 2007 Aug;6(2):128-40 [17512264.001]
  • [Cites] PLoS Med. 2007 Mar;4(3):e76 [17341128.001]
  • [Cites] Nat Genet. 1999 Nov;23(3):281-5 [10545947.001]
  • [Cites] EMBO J. 1999 Nov 15;18(22):6448-54 [10562556.001]
  • [Cites] Nature. 2000 Feb 17;403(6771):795-800 [10693811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 May 23;97(11):5807-11 [10811920.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6658-63 [10841563.001]
  • [Cites] FEBS Lett. 2000 Jun 23;475(3):237-41 [10869563.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jul 5;273(2):793-8 [10873683.001]
  • [Cites] Science. 2000 Sep 22;289(5487):2126-8 [11000115.001]
  • [Cites] FASEB J. 2000 Nov;14(14):2135-7 [11024000.001]
  • [Cites] FEMS Microbiol Rev. 2001 Jan;25(1):15-37 [11152939.001]
  • [Cites] Nature. 2001 Mar 8;410(6825):227-30 [11242085.001]
  • [Cites] EMBO J. 2001 Jan 15;20(1-2):197-209 [11226170.001]
  • [Cites] Science. 2001 Apr 13;292(5515):288-90 [11292860.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3514-22 [11313477.001]
  • [Cites] EMBO J. 2001 Aug 15;20(16):4522-35 [11500379.001]
  • [Cites] Mol Cell. 2001 Jul;8(1):45-55 [11511359.001]
  • [Cites] Int J Med Microbiol. 2001 Aug;291(3):219-25 [11554562.001]
  • [Cites] Mol Cell. 2001 Sep;8(3):489-98 [11583612.001]
  • [Cites] Genes Dev. 1997 Jan 15;11(2):241-54 [9009206.001]
  • [Cites] Genes Dev. 1997 Jan 15;11(2):255-69 [9009207.001]
  • [Cites] Science. 1997 Aug 29;277(5330):1313-6 [9271578.001]
  • [Cites] Cell. 1997 Dec 26;91(7):1033-42 [9428525.001]
  • [Cites] Mech Ageing Dev. 2006 Jan;127(1):48-56 [16280150.001]
  • [Cites] Science. 2005 Dec 9;310(5754):1641 [16339438.001]
  • [Cites] Genes Dev. 2006 Jan 15;20(2):174-84 [16418483.001]
  • [Cites] PLoS Genet. 2005 Nov;1(5):e69 [16311627.001]
  • [Cites] Annu Rev Biochem. 2006;75:435-65 [16756498.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10224-9 [16788062.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10230-5 [16790548.001]
  • [Cites] Curr Biol. 2006 Jul 11;16(13):1280-9 [16815704.001]
  • [Cites] Nat Struct Mol Biol. 2006 Jul;13(7):582-8 [16783377.001]
  • [Cites] J Neurosci. 2006 Aug 16;26(33):8484-91 [16914673.001]
  • [Cites] Cell. 2006 Sep 8;126(5):941-54 [16959573.001]
  • [Cites] Mol Biol Cell. 2006 Dec;17(12):5287-97 [17035629.001]
  • [Cites] EMBO Rep. 2006 Dec;7(12):1247-51 [17110954.001]
  • [Cites] Nature. 2006 Dec 14;444(7121):868-74 [17167475.001]
  • [Cites] Trends Biochem Sci. 2007 Jan;32(1):12-9 [17161604.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6161-71 [17200108.001]
  • [Cites] Cell Mol Life Sci. 2007 Mar;64(6):752-67 [17260088.001]
  • [Cites] FASEB J. 2007 Apr;21(4):1271-5 [17215485.001]
  • [Cites] PLoS Biol. 2007 Oct 2;5(10):e261 [17914901.001]
  • [Cites] PLoS Biol. 2007 Oct 2;5(10):e263 [17914902.001]
  • [Cites] Cell Metab. 2007 Nov;6(5):363-75 [17983582.001]
  • [Cites] PLoS Genet. 2008 Jan;4(1):e13 [18225956.001]
  • [Cites] Genes Dev. 2008 Apr 1;22(7):931-44 [18381895.001]
  • [Cites] Nature. 2008 Apr 17;452(7189):887-91 [18344983.001]
  • [Cites] Cell. 2008 May 16;133(4):627-39 [18485871.001]
  • [Cites] Biochim Biophys Acta. 2008 Jul;1783(7):1280-5 [18445486.001]
  • [Cites] Genes Dev. 2008 Jul 1;22(13):1753-7 [18550784.001]
  • [Cites] Annu Rev Nutr. 2008;28:115-30 [18429699.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18764-9 [19020097.001]
  • [Cites] PLoS One. 2009;4(4):e5212 [19381334.001]
  • [Cites] Nature. 2009 Jun 11;459(7248):802-7 [19516333.001]
  • [Cites] J Biol Chem. 2009 Jun 19;284(25):17110-9 [19416965.001]
  • [Cites] J Clin Invest. 2004 May;113(9):1318-27 [15124023.001]
  • [Cites] Genome Biol. 2004;5(5):224 [15128440.001]
  • [Cites] Cell. 2004 May 14;117(4):441-53 [15137938.001]
  • [Cites] Cell. 2004 May 14;117(4):495-502 [15137942.001]
  • [Cites] Nature. 2004 Jun 17;429(6993):771-6 [15175761.001]
  • [Cites] Science. 2004 Jul 16;305(5682):390-2 [15205477.001]
  • [Cites] Biochemistry. 2004 Aug 3;43(30):9877-87 [15274642.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):6931-46 [15282295.001]
  • [Cites] J Biol Chem. 2001 Oct 19;276(42):38837-43 [11483616.001]
  • [Cites] Cell. 2001 Oct 19;107(2):137-48 [11672522.001]
  • [Cites] Cell. 2001 Oct 19;107(2):149-59 [11672523.001]
  • [Cites] Yeast. 2002 Feb;19(3):215-24 [11816029.001]
  • [Cites] Genetics. 2002 Mar;160(3):877-89 [11901108.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18881-90 [11884393.001]
  • [Cites] FEBS Lett. 2002 Apr 24;517(1-3):97-102 [12062417.001]
  • [Cites] Nature. 2002 Jul 18;418(6895):344-8 [12124627.001]
  • [Cites] Science. 2002 Aug 2;297(5582):811 [12161648.001]
  • [Cites] Exp Gerontol. 2002 Aug-Sep;37(8-9):1023-30 [12213553.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):34489-98 [12091395.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(22):8056-66 [12391171.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45099-107 [12297502.001]
  • [Cites] Science. 2002 Dec 20;298(5602):2390-2 [12493915.001]
  • [Cites] Trends Biochem Sci. 2003 Jan;28(1):41-8 [12517451.001]
  • [Cites] Mol Cell. 2003 Feb;11(2):437-44 [12620231.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1751-3 [12610228.001]
  • [Cites] Curr Opin Cell Biol. 2003 Apr;15(2):241-6 [12648681.001]
  • [Cites] Nature. 2003 May 8;423(6936):181-5 [12736687.001]
  • [Cites] Biochemistry. 2003 Aug 12;42(31):9249-56 [12899610.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):7044-54 [12972620.001]
  • [Cites] Science. 2003 Dec 19;302(5653):2124-6 [14605207.001]
  • [Cites] Genes Dev. 2004 Jan 1;18(1):12-6 [14724176.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):1301-12 [14729974.001]
  • (PMID = 19818879.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG024351-02; United States / NIA NIH HHS / AG / AG024351-05; United States / BHP HRSA HHS / AH / R01-AH24351; United States / NIA NIH HHS / AG / AG024351-01; United States / NIA NIH HHS / AG / AG024351-02; United States / NIA NIH HHS / AG / R01 AG024351-03; United States / NIA NIH HHS / AG / AG024351-03; United States / NIA NIH HHS / AG / R01 AG024351-04; United States / NIA NIH HHS / AG / AG024351-04; United States / NIA NIH HHS / AG / R01 AG024351-05; United States / NIA NIH HHS / AG / R01 AG024351-01; United States / NIA NIH HHS / AG / R01 AG024351
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Silent Information Regulator Proteins, Saccharomyces cerevisiae; 0U46U6E8UK / NAD; EC 3.5.1.- / SIR2 protein, S cerevisiae; EC 3.5.1.- / Sirtuin 2
  • [Number-of-references] 132
  • [Other-IDs] NLM/ NIHMS151397; NLM/ PMC2886167
  •  go-up   go-down


78. Rossolillo P, Marinoni I, Galli E, Colosimo A, Albertini AM: YrxA is the transcriptional regulator that represses de novo NAD biosynthesis in Bacillus subtilis. J Bacteriol; 2005 Oct;187(20):7155-60
Hazardous Substances Data Bank. NICOTINIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] YrxA is the transcriptional regulator that represses de novo NAD biosynthesis in Bacillus subtilis.
  • The first genetic, in vivo, and in vitro evidences that YrxA is the regulator of NAD de novo biosynthesis in Bacillus subtilis are hereby reported.
  • [MeSH-major] Bacillus subtilis / genetics. Bacillus subtilis / metabolism. Genes, Bacterial / physiology. NAD / biosynthesis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Protein Expr Purif. 2000 Feb;18(1):64-70 [10648170.001]
  • [Cites] Microbiology. 1998 Nov;144 ( Pt 11):3097-104 [9846745.001]
  • [Cites] Vitam Horm. 2001;61:103-19 [11153263.001]
  • [Cites] J Mol Biol. 2001 Apr 13;307(5):1271-92 [11292341.001]
  • [Cites] Science. 2001 Oct 26;294(5543):849-52 [11679669.001]
  • [Cites] Science. 2002 Jun 14;296(5575):2028-33 [12004073.001]
  • [Cites] Drug Discov Today. 2003 Apr 15;8(8):335-6 [12681931.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4678-83 [12682299.001]
  • [Cites] Nature. 2003 May 1;423(6935):81-6 [12721629.001]
  • [Cites] Nature. 2003 May 1;423(6935):87-91 [12721630.001]
  • [Cites] J Bacteriol. 2003 Aug;185(16):4844-50 [12897004.001]
  • [Cites] Biochemistry. 2003 Oct 28;42(42):12430-8 [14567704.001]
  • [Cites] Genome Biol. 2004;5(10):R77 [15461803.001]
  • [Cites] Biochim Biophys Acta. 1968 Feb 1;156(1):77-84 [4296374.001]
  • [Cites] Biochim Biophys Acta. 1973 Apr 28;304(2):309-15 [4351074.001]
  • [Cites] J Bacteriol. 1975 Jan;121(1):212-8 [163810.001]
  • [Cites] Eur J Biochem. 1975 May;54(1):239-45 [238844.001]
  • [Cites] J Biol Chem. 1982 Jan 25;257(2):626-32 [7033218.001]
  • [Cites] J Gen Microbiol. 1985 Oct;131(10):2759-70 [3934331.001]
  • [Cites] Mol Gen Genet. 1987 Jun;208(1-2):279-87 [3039308.001]
  • [Cites] J Bacteriol. 1988 May;170(5):2113-20 [2834324.001]
  • [Cites] Eur J Biochem. 1988 Aug 1;175(2):221-8 [2841129.001]
  • [Cites] J Bacteriol. 1999 Jan;181(2):648-55 [9882682.001]
  • [Cites] Structure. 1999 Jul 15;7(7):745-56 [10425677.001]
  • [Cites] J Bacteriol. 1999 Sep;181(17):5509-11 [10464228.001]
  • [Cites] J Bacteriol. 1950 Jul;60(1):17-28 [15436457.001]
  • [Cites] J Bacteriol. 2005 Apr;187(8):2774-82 [15805524.001]
  • [Cites] Biol Chem Hoppe Seyler. 1990 Mar;371(3):239-48 [2187483.001]
  • [Cites] J Bacteriol. 1991 Feb;173(3):1311-20 [1991724.001]
  • [Cites] Genetics. 1991 Apr;127(4):657-70 [2029967.001]
  • [Cites] J Bacteriol. 1993 Mar;175(5):1423-32 [8444804.001]
  • [Cites] J Biol Chem. 1995 Mar 17;270(11):6181-5 [7890752.001]
  • [Cites] Nature. 1997 Nov 20;390(6657):249-56 [9384377.001]
  • [Cites] J Bacteriol. 1998 Sep;180(17):4739-41 [9721319.001]
  • [Cites] Nucleic Acids Res. 2000 Nov 1;28(21):4317-31 [11058132.001]
  • (PMID = 16199587.001).
  • [ISSN] 0021-9193
  • [Journal-full-title] Journal of bacteriology
  • [ISO-abbreviation] J. Bacteriol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / nifS protein, Bacteria; 0U46U6E8UK / NAD; 2679MF687A / Niacin; EC 2.4.2.- / Pentosyltransferases; EC 6.3.4.21 / nicotinate phosphoribosyltransferase
  • [Other-IDs] NLM/ PMC1251630
  •  go-up   go-down


79. Sporty J, Lin SJ, Kato M, Ognibene T, Stewart B, Turteltaub K, Bench G: Quantitation of NAD+ biosynthesis from the salvage pathway in Saccharomyces cerevisiae. Yeast; 2009 Jul;26(7):363-9
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitation of NAD+ biosynthesis from the salvage pathway in Saccharomyces cerevisiae.
  • Nicotinamide adenine dinucleotide (NAD+) is synthesized via two major pathways in prokaryotic and eukaryotic systems: the de novo biosynthesis pathway from tryptophan precursors, or the salvage biosynthesis pathway from either extracellular nicotinic acid or various intracellular NAD+ decomposition products.
  • NAD+ biosynthesis via the salvage pathway has been linked to an increase in yeast replicative lifespan under calorie restriction (CR).
  • However, the relative contribution of each pathway to NAD+ biosynthesis under both normal and CR conditions is not known.
  • Here, we have performed lifespan, NAD+ and NADH (the reduced form of NAD+) analyses on BY4742 wild-type, NAD+ salvage pathway knockout (npt1Delta) and NAD+ de novo pathway knockout (qpt1Delta) yeast strains cultured in media containing either 2% glucose (normal growth) or 0.5% glucose (CR).
  • We have utilized 14C labelled nicotinic acid in the culture media combined with HPLC speciation and both UV and 14C detection to quantitate the total amounts of NAD+ and NADH and the amounts derived from the salvage pathway.
  • We observed that wild-type and qpt1Delta yeast exclusively utilized extracellular nicotinic acid for NAD+ and NADH biosynthesis under both the 2% and 0.5% glucose growth conditions, suggesting that the de novo pathway plays little role if a functional salvage pathway is present.
  • We also observed that NAD+ concentrations decreased in all three strains under CR.
  • However, unlike the wild-type strain, NADH concentrations did not decrease and NAD+: NADH ratios did not increase under CR for either knockout strain.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLUCOSE .
  • Hazardous Substances Data Bank. NICOTINIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19399913.001).
  • [ISSN] 1097-0061
  • [Journal-full-title] Yeast (Chichester, England)
  • [ISO-abbreviation] Yeast
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P41 RR013461; United States / NIGMS NIH HHS / GM / P41 GM103483; United States / NCRR NIH HHS / RR / RR013461-11; United States / NCRR NIH HHS / RR / P41 RR013461-11; United States / NIA NIH HHS / AG / R01 AG024351
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 0 / Culture Media; 0U46U6E8UK / NAD; 2679MF687A / Niacin; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.19 / nicotinate-nucleotide diphosphorylase (carboxylating); EC 6.3.4.21 / nicotinate phosphoribosyltransferase; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS170938; NLM/ PMC4409826
  •  go-up   go-down


80. Tachibana S, Naka N, Kawai F, Yasuda M: Purification and characterization of cytoplasmic NAD-dependent polypropylene glycol dehydrogenase from Stenotrophomonas maltophilia. FEMS Microbiol Lett; 2008 Nov;288(2):266-72
Hazardous Substances Data Bank. Polypropylene glycol .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Purification and characterization of cytoplasmic NAD-dependent polypropylene glycol dehydrogenase from Stenotrophomonas maltophilia.
  • The oxidizing enzyme NAD(+)-dependent polypropylene glycol dehydrogenase (PPG-DH) was purified to homogeneity from the cytoplasmic fraction of Stenotrophomonas maltophilia grown on polypropylene glycol (diol type) 2000.
  • The purified enzyme consisted of a homotetrameric protein (37 kDa subunit) with a molecular mass of around 154 kDa.
  • The N-terminal amino acid sequence (25 residues) showed similarity to the sequences of NAD(+)-dependent secondary alcohol dehydrogenases and NADH-dependent reductases.
  • Consequently, the enzyme was classified into a group of NAD(+)-dependent secondary alcohol dehydrogenases.
  • [MeSH-major] Alcohol Dehydrogenase. NAD / metabolism. Polymers / metabolism. Propylene Glycols / metabolism. Stenotrophomonas maltophilia / enzymology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19054086.001).
  • [ISSN] 0378-1097
  • [Journal-full-title] FEMS microbiology letters
  • [ISO-abbreviation] FEMS Microbiol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Polymers; 0 / Propylene Glycols; 0U46U6E8UK / NAD; 25322-69-4 / polypropylene glycol; EC 1.1.1.1 / Alcohol Dehydrogenase
  •  go-up   go-down


81. Hara N, Yamada K, Shibata T, Osago H, Hashimoto T, Tsuchiya M: Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells. J Biol Chem; 2007 Aug 24;282(34):24574-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells.
  • NAD plays critical roles in various biological processes through the function of SIRT1.
  • Although classical studies in mammals showed that nicotinic acid (NA) is a better precursor than nicotinamide (Nam) in elevating tissue NAD levels, molecular details of NAD synthesis from NA remain largely unknown.
  • We here identified NA phosphoribosyltransferase (NAPRT) in humans and provided direct evidence of tight link between NAPRT and the increase in cellular NAD levels.
  • The enzyme was abundantly expressed in the small intestine, liver, and kidney in mice and mediated [(14)C]NAD synthesis from [(14)C]NA in human cells.
  • In cells expressing endogenous NAPRT, the addition of NA but not Nam almost doubled cellular NAD contents and decreased cytotoxicity by H(2)O(2).
  • These results indicate that NAPRT is essential for NA to increase cellular NAD levels and, thus, to prevent oxidative stress of the cells.
  • Kinetic analyses revealed that NAPRT, but not Nam phosphoribosyltransferase (NamPRT, also known as pre-B-cell colony-enhancing factor or visfatin), is insensitive to the physiological concentration of NAD.
  • Together, we conclude that NA elevates cellular NAD levels through NAPRT function and, thus, protects the cells against stress, partly due to lack of feedback inhibition of NAPRT but not NamPRT by NAD.
  • The ability of NA to increase cellular NAD contents may account for some of the clinically observed effects of the vitamin and further implies a novel application of the vitamin to treat diseases such as those associated with the depletion of cellular NAD pools.
  • [MeSH-major] NAD / metabolism. Niacin / metabolism. Pentosyltransferases / metabolism

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. NICOTINIC ACID .
  • SciCrunch. HGNC: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17604275.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB242230
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0U46U6E8UK / NAD; 2679MF687A / Niacin; EC 2.4.2.- / Pentosyltransferases; EC 6.3.4.21 / nicotinate phosphoribosyltransferase
  •  go-up   go-down


82. Martins AG, Constantin J, Bracht F, Kelmer-Bracht AM, Bracht A: The action of extracellular NAD+ on gluconeogenesis in the perfused rat liver. Mol Cell Biochem; 2006 Jun;286(1-2):115-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The action of extracellular NAD+ on gluconeogenesis in the perfused rat liver.
  • In the rat liver NAD+ infusion produces increases in portal perfusion pressure and glycogenolysis and transient inhibition of oxygen consumption.
  • NAD+ infusion into the portal vein (antegrade perfusion) produced a concentration-dependent (25-100 microM) transient inhibition of oxygen uptake and gluconeogenesis.
  • NAD+ infusion into the hepatic vein (retrograde perfusion) produced only transient stimulations.
  • During Ca2+-free perfusion the action of NAD+ was restricted to small transient stimulations.
  • Inhibitors of eicosanoid synthesis with different specificities (indo-methacin, nordihydroguaiaretic acid, bromophenacyl bromide) either inhibited or changed the action of NAD+.
  • The action of NAD+ on gluconeogenesis is probably mediated by eicosanoids synthesized in non-parenchymal cells.
  • As in the fed state, in the fasted condition extracellular NAD+ is also able to exert two opposite effects, inhibition and stimulation.
  • [MeSH-major] Gluconeogenesis / drug effects. Liver / drug effects. NAD / pharmacology

  • Hazardous Substances Data Bank. LACTIC ACID .
  • Hazardous Substances Data Bank. GLUCOSE .
  • Hazardous Substances Data Bank. INDOMETHACIN .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16652226.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Antioxidants; 0 / Enzyme Inhibitors; 0U46U6E8UK / NAD; 33X04XA5AT / Lactic Acid; 7BO8G1BYQU / Masoprocol; EC 3.1.1.- / Phospholipases A; IY9XDZ35W2 / Glucose; PN0FRW1G4Z / 4-bromophenacyl bromide; SY7Q814VUP / Calcium; XXE1CET956 / Indomethacin
  •  go-up   go-down


83. Tronconi MA, Gerrard Wheeler MC, Maurino VG, Drincovich MF, Andreo CS: NAD-malic enzymes of Arabidopsis thaliana display distinct kinetic mechanisms that support differences in physiological control. Biochem J; 2010 Sep 1;430(2):295-303
The Arabidopsis Information Resource. Linked Gene Data (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD-malic enzymes of Arabidopsis thaliana display distinct kinetic mechanisms that support differences in physiological control.
  • The Arabidopsis thaliana genome contains two genes encoding NAD-MEs [NAD-dependent malic enzymes; NAD-ME1 (TAIR accession number At4G13560) and NAD-ME2 (TAIR accession number At4G00570)].
  • In the present work, the kinetic mechanisms of NAD-ME1 and -ME2 homodimers and NAD-MEH (NAD-ME heterodimer) were studied as an approach to understand the contribution of these enzymes to plant physiology.
  • Product-inhibition and substrate-analogue analyses indicated that NAD-ME2 follows a sequential ordered Bi-Ter mechanism, NAD being the leading substrate followed by L-malate.
  • On the other hand, NAD-ME1 and NAD-MEH can bind both substrates randomly.
  • However, NAD-ME1 shows a preferred route that involves the addition of NAD first.
  • As a consequence of the kinetic mechanism, NAD-ME1 showed a partial inhibition by L-malate at low NAD concentrations.
  • The analysis of a protein chimaeric for NAD-ME1 and -ME2 indicated that the first 176 amino acids are associated with the differences observed in the kinetic mechanisms of the enzymes.
  • Furthermore, NAD-ME1, -ME2 and -MEH catalyse the reverse reaction (pyruvate reductive carboxylation) with very low catalytic activity, supporting the notion that these isoforms act only in L-malate oxidation in plant mitochondria.
  • The different kinetic mechanism of each NAD-ME entity suggests that, for a metabolic condition in which the mitochondrial NAD level is low and the L-malate level is high, the activity of NAD-ME2 and/or -MEH would be preferred over that of NAD-ME1.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20528775.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arabidopsis Proteins; EC 1.1.1.37 / Malate Dehydrogenase; EC 1.1.1.38 / malate dehydrogenase-(oxaloacetate-decarboxylating) (NAD+)
  •  go-up   go-down


84. Haag F, Adriouch S, Braß A, Jung C, Möller S, Scheuplein F, Bannas P, Seman M, Koch-Nolte F: Extracellular NAD and ATP: Partners in immune cell modulation. Purinergic Signal; 2007 Mar;3(1-2):71-81

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extracellular NAD and ATP: Partners in immune cell modulation.
  • Extracellular NAD and ATP exert multiple, partially overlapping effects on immune cells.
  • ATP and its metabolites signal through purinergic P2 and P1 receptors, whereas extracellular NAD exerts its effects by serving as a substrate for ADP-ribosyltransferases (ARTs) and NAD glycohydrolases/ADPR cyclases like CD38 and CD157.
  • While ATP activates P2X7 directly as a soluble ligand, activation via NAD occurs by ART-dependent ADP-ribosylation of cell surface proteins, providing an immobilised ligand.
  • Activation by ATP requires high micromolar concentrations of nucleotide and is readily reversible, whereas NAD-dependent stimulation begins at low micromolar concentrations and is more stable.
  • Under conditions of cell stress or inflammation, ATP and NAD are released into the extracellular space from intracellular stores by lytic and non-lytic mechanisms, and may serve as "danger signals" to alert the immune response to tissue damage.
  • Since ART expression is limited to naïve/resting T cells, P2X7-mediated NAD-induced cell death (NICD) specifically targets this cell population.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2001 Feb 9;276(6):3820-6 [11056157.001]
  • [Cites] J Biol Chem. 2001 Apr 6;276(14):11135-42 [11150303.001]
  • [Cites] Pharmacol Rev. 2001 Mar;53(1):107-18 [11171941.001]
  • [Cites] FEBS Lett. 2001 Mar 9;492(1-2):4-8 [11248227.001]
  • [Cites] Mutat Res. 2001 Jun 2;477(1-2):97-110 [11376691.001]
  • [Cites] J Immunol. 2001 Jun 15;166(12):7172-7 [11390464.001]
  • [Cites] J Immunol. 2001 Jul 1;167(1):196-203 [11418649.001]
  • [Cites] Neurochem Res. 2001 Sep;26(8-9):959-69 [11699948.001]
  • [Cites] Biochem J. 2002 Oct 1;367(Pt 1):121-8 [12099890.001]
  • [Cites] Eur J Immunol. 2002 Sep;32(9):2409-17 [12207325.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(21):7535-42 [12370300.001]
  • [Cites] J Immunol. 2002 Oct 15;169(8):4108-12 [12370338.001]
  • [Cites] Blood. 2003 May 15;101(10):3985-90 [12446452.001]
  • [Cites] J Leukoc Biol. 2003 Mar;73(3):339-43 [12629147.001]
  • [Cites] Biochem J. 1998 Mar 15;330 ( Pt 3):1383-90 [9494110.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1324-33 [9694721.001]
  • [Cites] Pharmacol Rev. 1998 Sep;50(3):413-92 [9755289.001]
  • [Cites] Immunity. 2001 Nov;15(5):825-35 [11728343.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):495-500 [11756680.001]
  • [Cites] Blood. 2002 Jan 15;99(2):706-8 [11781259.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10482-8 [11790776.001]
  • [Cites] Nat Med. 2002 Apr;8(4):358-65 [11927941.001]
  • [Cites] Lancet. 2002 Mar 30;359(9312):1114-9 [11943260.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8231-5 [12060767.001]
  • [Cites] Protein Sci. 2002 Jul;11(7):1657-70 [12070318.001]
  • [Cites] Anal Biochem. 2003 Mar 1;314(1):108-15 [12633608.001]
  • [Cites] Mol Pharmacol. 2003 Apr;63(4):773-6 [12644576.001]
  • [Cites] Blood. 2003 Jul 15;102(2):613-20 [12649135.001]
  • [Cites] Can J Vet Res. 2003 Jul;67(3):229-31 [12889731.001]
  • [Cites] Biochim Biophys Acta. 2003 Sep 2;1615(1-2):7-32 [12948585.001]
  • [Cites] Immunity. 2003 Sep;19(3):403-12 [14499115.001]
  • [Cites] Immunity. 2003 Oct;19(4):571-82 [14563321.001]
  • [Cites] J Neurosci. 2004 Jan 7;24(1):1-7 [14715932.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Dec;295(3):862-9 [11082418.001]
  • [Cites] Science. 1996 May 3;272(5262):735-8 [8614837.001]
  • [Cites] Immunity. 2004 Mar;20(3):279-91 [15030772.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9479-84 [15194822.001]
  • [Cites] Biochem J. 2005 Jan 1;385(Pt 1):309-17 [15361073.001]
  • [Cites] J Biol Chem. 2004 Nov 19;279(47):48893-903 [15364945.001]
  • [Cites] J Physiol. 2004 Dec 1;561(Pt 2):499-513 [15579539.001]
  • [Cites] J Bone Miner Res. 2005 Jan;20(1):41-9 [15619668.001]
  • [Cites] J Immunol. 2005 Mar 15;174(6):3298-305 [15749861.001]
  • [Cites] Mol Biol Cell. 2005 Jul;16(7):3100-6 [15843434.001]
  • [Cites] Mol Biol Cell. 2005 Aug;16(8):3659-65 [15944221.001]
  • [Cites] Br J Pharmacol. 2005 Oct;146(3):435-44 [15997228.001]
  • [Cites] Nat Rev Immunol. 2005 Sep;5(9):712-21 [16110315.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):3075-83 [16116196.001]
  • [Cites] Cell Immunol. 2005 Jul-Aug;236(1-2):59-65 [16168396.001]
  • [Cites] Purinergic Signal. 2005 Sep;1(3):205-9 [18404505.001]
  • [Cites] J Biol Chem. 1996 Mar 29;271(13):7686-93 [8631807.001]
  • [Cites] Trends Pharmacol Sci. 1997 Mar;18(3):79-82 [9133776.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1600-10 [9269779.001]
  • [Cites] J Biol Chem. 1997 Oct 10;272(41):25881-9 [9325320.001]
  • [Cites] Cell Biochem Biophys. 1998;28(1):45-62 [9386892.001]
  • [Cites] Lab Invest. 1998 Nov;78(11):1375-83 [9840612.001]
  • [Cites] Biofactors. 1998;8(3-4):301-3 [9914832.001]
  • [Cites] Cell Death Differ. 1998 Mar;5(3):191-9 [10200464.001]
  • [Cites] Eur J Biochem. 1999 Jun;262(2):342-8 [10336617.001]
  • [Cites] Biochem J. 1999 Sep 1;342 ( Pt 2):249-68 [10455009.001]
  • [Cites] J Mol Med (Berl). 2000;78(1):26-35 [10759027.001]
  • [Cites] FASEB J. 2001 Jan;15(1):10-12 [11099492.001]
  • [Cites] Blood. 2001 Feb 1;97(3):587-600 [11157473.001]
  • [Cites] J Immunol. 2001 Feb 1;166(3):1611-7 [11160202.001]
  • [Cites] FASEB J. 2001 Sep;15(11):1963-70 [11532976.001]
  • [Cites] J Immunol. 2001 Sep 15;167(6):3300-7 [11544318.001]
  • [Cites] J Biotechnol. 2001 Dec 28;92(2):81-7 [11640979.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1715-22 [11861288.001]
  • [Cites] Blood. 2005 May 1;105(9):3663-70 [15657180.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36334-41 [16118205.001]
  • [Cites] Cell Immunol. 2005 Jul-Aug;236(1-2):66-71 [16271711.001]
  • [Cites] Pharmacol Rev. 1972 Sep;24(3):509-81 [4404211.001]
  • [Cites] J Biol Chem. 1993 Dec 5;268(34):25273-6 [8244957.001]
  • [Cites] J Biol Chem. 1995 Dec 22;270(51):30327-33 [8530456.001]
  • [Cites] J Exp Med. 1997 Feb 3;185(3):579-82 [9053458.001]
  • [Cites] Immunity. 1997 Sep;7(3):433-44 [9324363.001]
  • [Cites] Electrophoresis. 1999 Jul;20(10):2111-7 [10451123.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2000;40:563-80 [10836147.001]
  • [Cites] J Immunol. 2000 Oct 15;165(8):4463-9 [11035085.001]
  • (PMID = 18404420.001).
  • [ISSN] 1573-9538
  • [Journal-full-title] Purinergic signalling
  • [ISO-abbreviation] Purinergic Signal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2096762
  •  go-up   go-down


85. Cai AL, Zipfel GJ, Sheline CT: Zinc neurotoxicity is dependent on intracellular NAD levels and the sirtuin pathway. Eur J Neurosci; 2006 Oct;24(8):2169-76
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zinc neurotoxicity is dependent on intracellular NAD levels and the sirtuin pathway.
  • We previously demonstrated that toxicity of extracellular Zn(2+) depended on entry, elevation in intracellular free Zn(2+) ([Zn(2+)](i)), a reduction in NAD(+) and ATP levels, and dysfunction of glycolysis and cellular metabolism.
  • We suggested that PARP-1 activation alone can not explain this loss of neuronal NAD(+).
  • NAD(+) was recently demonstrated to permeate neurons and glia, and we have now shown that exogenous NAD(+) can reduce Zn(2+) neurotoxicity, and 3-acetylpyridine, which generates inactive NAD(+), potentiated Zn(2+) neurotoxicity.
  • Sirtinol and 2-hydroxynaphthaldehyde, inhibitors of the sirtuin pathway (SIRT proteins are NAD(+)-catabolic protein deacetylases), attenuated both acute and chronic Zn(2+) neurotoxicity.
  • Resveratrol and fisetin (sirtuin activators) potentiated NAD(+) loss and Zn(2+) neurotoxicities.
  • Furthermore, neuronal cultures derived from the Wld(s) mouse, which overexpress the NAD(+) synthetic enzyme nicotinamide mononucleotide adenyl transferase (NMNAT-1), had reduced sensitivity to Zn(2+) neurotoxicity.
  • Finally, nicotinamide was demonstrated to attenuate CA1 neuronal death after 10 min of global ischemia in rat even if administered 1 h after the insult.
  • Together with previous data, these results further implicate NAD(+) levels in Zn(2+) neurotoxicity.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RESVERATROL .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17042794.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK073446; United States / NINDS NIH HHS / NS / R01 NS030337; United States / NIDDK NIH HHS / DK / DK 073446; United States / NINDS NIH HHS / NS / NS 030337
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 2-hydroxynaphthaldehyde; 0 / Aldehydes; 0 / Antioxidants; 0 / Flavonoids; 0 / Ion Channels; 0 / Naphthalenes; 0 / Neurotoxins; 0 / Pyridines; 0 / Stilbenes; 00QT8FX306 / 3-acetylpyridine; 0U46U6E8UK / NAD; 25X51I8RD4 / Niacinamide; EC 3.5.1.- / Sirtuins; J41CSQ7QDS / Zinc; OO2ABO9578 / fisetin; Q369O8926L / resveratrol
  •  go-up   go-down


86. Mani-Telang P, Sutrias-Grau M, Williams G, Arnosti DN: Role of NAD binding and catalytic residues in the C-terminal binding protein corepressor. FEBS Lett; 2007 Nov 13;581(27):5241-6
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of NAD binding and catalytic residues in the C-terminal binding protein corepressor.
  • These proteins are homologous to prokaryotic D-2-hydroxyacid dehydrogenases, possessing an NAD/NADH binding fold and conserved active site residues.
  • When expressed in Drosophila, a catalytic site mutant retains biological activity, however, we find that an NAD binding mutant lacks biological activity.
  • The NAD mutant, similar to a dimerization mutant, is expressed at low levels, indicating that binding of NAD/NADH may affect CtBP stability.
  • These data support the idea that the ancestral dehydrogenase activity is not required for CtBP function, and NAD binding may play a regulatory, rather than catalytic, role.
  • [MeSH-major] Alcohol Oxidoreductases / chemistry. Alcohol Oxidoreductases / metabolism. DNA-Binding Proteins / chemistry. DNA-Binding Proteins / metabolism. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17964573.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM56976
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Drosophila Proteins; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0U46U6E8UK / NAD; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein
  •  go-up   go-down


87. Young GS, Choleris E, Lund FE, Kirkland JB: Decreased cADPR and increased NAD+ in the Cd38-/- mouse. Biochem Biophys Res Commun; 2006 Jul 21;346(1):188-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decreased cADPR and increased NAD+ in the Cd38-/- mouse.
  • CD38 is a type II glycoprotein that catalyzes the formation of cyclic ADP-ribose (cADPR), an intracellular calcium signalling molecule, from nicotinamide adenine dinucleotide (NAD(+)).
  • We also report significant increases in brain, lung, and kidney NAD(+) in the Cd38(-/-) mouse, and provide the first experimental demonstration of the proximate relationship between CD38 and NAD(+).
  • [MeSH-major] Antigens, CD38 / deficiency. Cyclic ADP-Ribose / metabolism. Membrane Glycoproteins / deficiency. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16750163.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0U46U6E8UK / NAD; 119340-53-3 / Cyclic ADP-Ribose; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / Cd38 protein, mouse
  •  go-up   go-down


88. Boshoff HI, Xu X, Tahlan K, Dowd CS, Pethe K, Camacho LR, Park TH, Yun CS, Schnappinger D, Ehrt S, Williams KJ, Barry CE 3rd: Biosynthesis and recycling of nicotinamide cofactors in mycobacterium tuberculosis. An essential role for NAD in nonreplicating bacilli. J Biol Chem; 2008 Jul 11;283(28):19329-41
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biosynthesis and recycling of nicotinamide cofactors in mycobacterium tuberculosis. An essential role for NAD in nonreplicating bacilli.
  • Despite the presence of genes that apparently encode NAD salvage-specific enzymes in its genome, it has been previously thought that Mycobacterium tuberculosis can only synthesize NAD de novo.
  • Transcriptional analysis of the de novo synthesis and putative salvage pathway genes revealed an up-regulation of the salvage pathway genes in vivo and in vitro under conditions of hypoxia.
  • [14C]Nicotinamide incorporation assays in M. tuberculosis isolated directly from the lungs of infected mice or from infected macrophages revealed that incorporation of exogenous nicotinamide was very efficient in in vivo-adapted cells, in contrast to cells grown aerobically in vitro.
  • Mutants in the de novo pathway died upon removal of exogenous nicotinamide during active replication in vitro.
  • Cell death is induced by both cofactor starvation and disruption of cellular redox homeostasis as electron transport is impaired by limiting NAD.
  • Inhibitors of NAD synthetase, an essential enzyme common to both recycling and de novo synthesis pathways, displayed the same bactericidal effect as sudden NAD starvation of the de novo pathway mutant in both actively growing and nonreplicating M. tuberculosis.
  • These studies demonstrate the plasticity of the organism in maintaining NAD levels and establish that the two enzymes of the universal pathway are attractive chemotherapeutic targets for active as well as latent tuberculosis.