[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 5580
6. Srivastava SK, Dube D, Kukshal V, Jha AK, Hajela K, Ramachandran R: NAD+-dependent DNA ligase (Rv3014c) from Mycobacterium tuberculosis: novel structure-function relationship and identification of a specific inhibitor. Proteins; 2007 Oct 1;69(1):97-111
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+-dependent DNA ligase (Rv3014c) from Mycobacterium tuberculosis: novel structure-function relationship and identification of a specific inhibitor.
  • Mycobacterium tuberculosis codes for an essential NAD+-dependent DNA ligase (MtuLigA) which is a novel, validated, and attractive drug target.
  • We also report the identification, through virtual screening, of a novel N-substituted tetracyclic indole that competes with NAD+ and inhibits the enzyme with IC50 in the low muM range.
  • In silico ligand-docking studies suggest that the exquisite specificity of the inhibitor arises on account of its mimicking the interactions of NAD+ with MtuLigA.

  • BindingDB. BindingDB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17557328.001).
  • [ISSN] 1097-0134
  • [Journal-full-title] Proteins
  • [ISO-abbreviation] Proteins
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Indoles; EC 6.5.1.- / DNA Ligases; EC 6.5.1.2 / DNA ligase (NAD)
  •  go-up   go-down


7. Bragg JW, Swindle L, Halpern AC, Marghoob AA: Agminated acquired melanocytic nevi of the common and dysplastic type. J Am Acad Dermatol; 2005 Jan;52(1):67-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Agminated acquired melanocytic nevi of the common and dysplastic type.
  • We previously reported a single case of agminated acquired melanocytic nevi, consisting of a localized clustering of banal and atypical moles.
  • We examined the lesions clinically, with a dermoscope, with a Wood's light, and in 3 cases with UV photography so as to exclude nevus spilus from the differential diagnosis.
  • The presence of an underlying dysplastic nevus syndrome phenotype in 4 of the 5 cases raises the possibility that agminated nevi arise as a consequence of postzygotic loss of heterozygosity and, thus, may represent a type 2 segmental manifestation of the atypical mole syndrome phenotype.
  • [MeSH-major] Nevus, Pigmented / pathology. Skin Neoplasms / pathology

  • 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 = 15627083.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


8. Hubackova M, Vaclavikova R, Mrhalova M, Kubackova K, Kodet R, Gut I, Soucek P: NAD(P)H:quinone oxidoreductase 1 Pro187Ser polymorphism and expression do not cosegregate with clinico-pathological characteristics of human mammary tumors. Pharmacogenet Genomics; 2009 Jul;19(7):505-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD(P)H:quinone oxidoreductase 1 Pro187Ser polymorphism and expression do not cosegregate with clinico-pathological characteristics of human mammary tumors.
  • OBJECTIVE: The aim of this study was to further clarify the recently reported role of NAD(P)H:quinone oxidoreductase 1 (NQO1) as a strong prognostic and predictive factor in breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Gene Expression Regulation, Neoplastic. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Single Nucleotide / genetics. Proline / genetics. Serine / genetics

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827856191 for PMID:19494791 [PharmGKB] .
  • Hazardous Substances Data Bank. (L)-PROLINE .
  • Hazardous Substances Data Bank. L-SERINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19494791.001).
  • [ISSN] 1744-6872
  • [Journal-full-title] Pharmacogenetics and genomics
  • [ISO-abbreviation] Pharmacogenet. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 452VLY9402 / Serine; 9DLQ4CIU6V / Proline; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  •  go-up   go-down


9. Lee SO, Chang YC, Whang K, Kim CH, Lee IS: Role of NAD(P)H:quinone oxidoreductase 1 on tumor necrosis factor-alpha-induced migration of human vascular smooth muscle cells. Cardiovasc Res; 2007 Nov 1;76(2):331-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of NAD(P)H:quinone oxidoreductase 1 on tumor necrosis factor-alpha-induced migration of human vascular smooth muscle cells.
  • OBJECTIVES: In a preliminary study, NAD(P)H:quinone oxidoreductase 1 (NQO1) was found to be highly expressed in cultured human aortic smooth muscle cells (HASMC) and dicumarol, a NQO1 inhibitor and a coumarin-derived natural anticoagulant, suppressed tumor necrosis factor (TNF)-alpha-induced HASMC migration.
  • [MeSH-major] Muscle, Smooth, Vascular / drug effects. Myocytes, Smooth Muscle / drug effects. NAD(P)H Dehydrogenase (Quinone) / physiology. Tumor Necrosis Factor-alpha / pharmacology

  • Hazardous Substances Data Bank. DICUMAROL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 17669387.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Matrix Metalloproteinase Inhibitors; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; 7QID3E7BG7 / Dicumarol; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


10. de Sousa NC, de Rezende AA, da Silva RM, Guterres ZR, Graf U, Kerr WE, Spanó MA: Modulatory effects of Tabebuia impetiginosa (Lamiales, Bignoniaceae) on doxorubicin-induced somatic mutation and recombination in Drosophila melanogaster. Genet Mol Biol; 2009 Apr;32(2):382-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • They induce apoptosis by generating oxygen-reactive species, thereby inhibiting topoisomerases (I and II) or inducing other enzymes dependent on NAD(P)H:quinone oxidoreductase 1, thus affecting cell cycle checkpoints.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Phytochemistry. 2005 Mar;66(5):589-97 [15721952.001]
  • [Cites] Mutat Res. 2006 Sep 5;607(2):225-30 [16777474.001]
  • [Cites] Bioorg Med Chem Lett. 2007 Dec 1;17(23):6417-20 [17950604.001]
  • [Cites] Food Chem Toxicol. 2008 Mar;46(3):1103-10 [18160198.001]
  • [Cites] Mutat Res. 1990 Jul;244(3):201-8 [2114542.001]
  • [Cites] Mutat Res. 1989 Jun;216(3):179-87 [2499781.001]
  • [Cites] Chem Pharm Bull (Tokyo). 2006 Jan;54(1):14-20 [16394542.001]
  • [Cites] Environ Mol Mutagen. 2003;41(4):293-9 [12717784.001]
  • [Cites] Mutagenesis. 2001 Sep;16(5):385-94 [11507237.001]
  • [Cites] Environ Mol Mutagen. 2000;36(3):195-200 [11044900.001]
  • [Cites] Phytochemistry. 2000 Apr;53(8):869-72 [10820794.001]
  • [Cites] Mutat Res. 2005 Aug 1;585(1-2):147-55 [16005256.001]
  • [Cites] Phytochemistry. 2004 Jul;65(13):2003-11 [15280007.001]
  • [Cites] Life Sci. 2004 Mar 12;74(17):2157-84 [14969719.001]
  • [Cites] Life Sci. 2004 Jan 9;74(8):935-68 [14672753.001]
  • [Cites] Mutat Res. 1992 Feb;271(1):59-67 [1371830.001]
  • [Cites] Genetics. 1977 Dec;87(4):685-97 [414959.001]
  • [Cites] Mutat Res. 1998 Jun 18;402(1-2):203-9 [9729134.001]
  • [Cites] J Ethnopharmacol. 1993 Jun;39(2):119-28 [8412245.001]
  • [Cites] Mutagenesis. 1994 Jul;9(4):383-6 [7968582.001]
  • [Cites] Mutat Res. 1995 Apr;334(2):247-58 [7885379.001]
  • [Cites] Environ Mutagen. 1984;6(2):153-88 [6423380.001]
  • [Cites] Cancer Res. 1983 Feb;43(2):460-72 [6293697.001]
  • [Cites] Mutat Res. 1988 Aug;203(4):297-308 [3136327.001]
  • [Cites] Mutat Res. 1989 Apr;222(4):359-73 [2495439.001]
  • [Cites] Drug Metab Dispos. 2008 Apr;36(4):753-8 [18227145.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Apr;61(5):739-49 [17594094.001]
  • [Cites] Mutat Res. 2007 Jan 10;626(1-2):1-3 [17141555.001]
  • [Cites] IARC Sci Publ. 1999;(146):427-70 [10353398.001]
  • [Cites] J Nat Prod. 1999 Aug;62(8):1134-6 [10479319.001]
  • [Cites] Mutat Res. 1999 Aug 18;444(2):355-65 [10521675.001]
  • [Cites] J Antimicrob Chemother. 2005 Dec;56(6):1034-41 [16269551.001]
  • [Cites] J Ethnopharmacol. 2006 Apr 21;105(1-2):255-62 [16359837.001]
  • [Cites] Mutat Res. 2003 Aug 5;539(1-2):167-75 [12948825.001]
  • (PMID = 21637695.001).
  • [ISSN] 1415-4757
  • [Journal-full-title] Genetics and molecular biology
  • [ISO-abbreviation] Genet. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3036921
  • [Keywords] NOTNLM ; genotoxicity / somatic mutation and recombination test - SMART / synergistic effect / toxicity / wing spot test
  •  go-up   go-down


11. Niemiec P, Zak I, Emich-Widera E, Balcerzyk A, Kopyta I, Nowak T, Wendorff J, Pałatyńska K, Kaciński M, Pienczk-Ręcławowicz K, Pilarska E: The C242T polymorphism of the gene encoding cytochrome b-245 alpha is not associated with paediatric ischaemic stroke: family-based and case-control study. Neurol Neurochir Pol; 2010 Sep-Oct;44(5):453-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cytochrome b-245 alpha gene (CYBA) encodes cytochrome b-245 alpha light chain (p22phox peptide), a critical element of NAD(P)H oxidases, the most important source of superoxide anion in the cerebral arteries.

  • MedlinePlus Health Information. consumer health - Ischemic Stroke.
  • MedlinePlus Health Information. consumer health - Stroke.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21082491.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] EC 1.6.3.1 / CYBA protein, human; EC 1.6.3.1 / NADPH Oxidase
  •  go-up   go-down


12. Pacher P, Szabo C: Role of the peroxynitrite-poly(ADP-ribose) polymerase pathway in human disease. Am J Pathol; 2008 Jul;173(1):2-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PARP overactivation depletes its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, eventually leading to functional impairment or death of cells, as well as up-regulation of various proinflammatory pathways.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Respir Crit Care Med. 1999 Sep;160(3):1031-4 [10471637.001]
  • [Cites] Oncogene. 2007 Dec 10;26(56):7816-24 [18066095.001]
  • [Cites] Int J Cardiol. 2008 Jan 24;123(3):366-8 [17689746.001]
  • [Cites] J Biol Chem. 2008 Jan 11;283(2):1197-208 [18025084.001]
  • [Cites] J Neurol. 2008 Jan;255(1):94-8 [18080850.001]
  • [Cites] Science. 2008 Feb 8;319(5864):819-21 [18258916.001]
  • [Cites] BMC Bioinformatics. 2007;8:483 [18093328.001]
  • [Cites] Int J Mol Med. 2008 Jul;22(1):113-8 [18575783.001]
  • [Cites] J Neurosurg. 2003 Jul;99(1):125-30 [12854754.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Jan;163(1):166-72 [11208643.001]
  • [Cites] Circulation. 2001 Jul 10;104(2):174-80 [11447082.001]
  • [Cites] Diabetologia. 2001 Jul;44(7):834-8 [11508267.001]
  • [Cites] Ann Thorac Surg. 2001 Aug;72(2):571-6 [11515899.001]
  • [Cites] Circulation. 2001 Sep 18;104(12 Suppl 1):I336-43 [11568079.001]
  • [Cites] J Heart Lung Transplant. 2003 Sep;22(9):1028-36 [12957613.001]
  • [Cites] Cardiovasc Res. 2003 Oct 15;60(1):108-18 [14522412.001]
  • [Cites] J Thorac Cardiovasc Surg. 2003 Dec;126(6):1813-21 [14688692.001]
  • [Cites] J Autoimmun. 2004 Feb;22(1):87-94 [14709417.001]
  • [Cites] Neurology. 2004 Jan 27;62(2):319-22 [14745081.001]
  • [Cites] Trends Pharmacol Sci. 2004 May;25(5):259-64 [15120492.001]
  • [Cites] Crit Care Med. 2006 Apr;34(4):1073-9 [16484919.001]
  • [Cites] J Vasc Surg. 2006 Apr;43(4):760-70; discussion 770-1 [16616233.001]
  • [Cites] Free Radic Biol Med. 2006 Apr 15;40(8):1454-65 [16631535.001]
  • [Cites] Rheumatology (Oxford). 2006 Jun;45(6):711-7 [16461442.001]
  • [Cites] Trends Biochem Sci. 2006 Jun;31(6):309-11 [16679020.001]
  • [Cites] Circulation. 2006 Jul 4;114(1 Suppl):I257-63 [16820582.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982.001]
  • [Cites] Curr Pharm Des. 2006;12(23):2903-10 [16918420.001]
  • [Cites] Free Radic Biol Med. 2006 Nov 1;41(9):1384-91 [17023265.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Nov 17;350(2):352-7 [17007818.001]
  • [Cites] Arch Dis Child Fetal Neonatal Ed. 2006 Nov;91(6):F429-33 [16835259.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 1;350(4):1056-62 [17046715.001]
  • [Cites] Arthritis Rheum. 2001 Dec;44(12):2909-21 [11762952.001]
  • [Cites] Diabetes Care. 2002 Aug;25(8):1439-43 [12145247.001]
  • [Cites] Circulation. 2002 Aug 20;106(8):927-32 [12186795.001]
  • [Cites] Diabetes. 2002 Sep;51(9):2817-25 [12196476.001]
  • [Cites] Basic Res Cardiol. 2002 Sep;97(5):409-15 [12200641.001]
  • [Cites] Pharmacol Rev. 2002 Sep;54(3):375-429 [12223530.001]
  • [Cites] Br J Pharmacol. 2003 Feb;138(4):532-43 [12598407.001]
  • [Cites] Arthritis Rheum. 2003 Mar;48(3):638-41 [12632415.001]
  • [Cites] Toxicol Lett. 2003 Apr 11;140-141:105-12 [12676456.001]
  • [Cites] J Neurochem. 2003 May;85(3):697-708 [12694396.001]
  • [Cites] Free Radic Biol Med. 2003 Jul 15;35(2):140-8 [12853070.001]
  • [Cites] Crit Rev Oral Biol Med. 2004;15(3):156-64 [15187033.001]
  • [Cites] Science. 2004 Jun 18;304(5678):1820-2 [15205535.001]
  • [Cites] Neuroreport. 2004 Aug 6;15(11):1715-8 [15257133.001]
  • [Cites] J Heart Lung Transplant. 2004 Jun;23(6):723-8 [15366433.001]
  • [Cites] Mol Med. 2004 Jan-Jun;10(1-6):28-35 [15502880.001]
  • [Cites] Clin Exp Immunol. 1979 Apr;36(1):151-64 [313859.001]
  • [Cites] Arthritis Rheum. 1989 Aug;32(8):1045-9 [2765003.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1620-4 [2154753.001]
  • [Cites] Autoimmunity. 1990;6(3):203-9 [2129778.001]
  • [Cites] Science. 1994 Feb 4;263(5147):687-9 [8080500.001]
  • [Cites] Clin Immunol Immunopathol. 1995 Dec;77(3):349-57 [7586746.001]
  • [Cites] J Immunol. 1996 Jan 1;156(1):350-8 [8598485.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Mar 5;93(5):1753-8 [8700830.001]
  • [Cites] Mol Cell Biochem. 1996 Oct-Nov;163-164:261-75 [8974066.001]
  • [Cites] Crit Care Med. 1997 May;25(5):812-9 [9187601.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3867-72 [9520459.001]
  • [Cites] Transplantation. 1998 Mar 27;65(6):804-12 [9539092.001]
  • [Cites] Circulation. 1998 Jun 16;97(23):2338-45 [9639378.001]
  • [Cites] Trends Pharmacol Sci. 1998 Jul;19(7):287-98 [9703762.001]
  • [Cites] Immunology. 1998 Jul;94(3):345-55 [9767416.001]
  • [Cites] Brain. 1999 Feb;122 ( Pt 2):247-53 [10071053.001]
  • [Cites] Neuropathol Appl Neurobiol. 1999 Apr;25(2):98-103 [10215997.001]
  • [Cites] Trends Pharmacol Sci. 2006 Dec;27(12):626-30 [17055069.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18314-9 [17116881.001]
  • [Cites] Am J Respir Cell Mol Biol. 2007 Feb;36(2):152-7 [17023686.001]
  • [Cites] Mol Med. 2006 Sep-Oct;12(9-10):221-8 [17225870.001]
  • [Cites] J Cell Biochem. 2007 Feb 1;100(2):385-401 [16924674.001]
  • [Cites] Physiol Rev. 2007 Jan;87(1):315-424 [17237348.001]
  • [Cites] Clin Nephrol. 2002 Aug;58(2):103-10 [12227681.001]
  • [Cites] Circulation. 2002 Nov 19;106(21):2680-6 [12438293.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Jan;62(1):88-103 [12528821.001]
  • [Cites] J Clin Invest. 2003 Jan;111(2):163-9 [12531868.001]
  • [Cites] J Thorac Cardiovasc Surg. 2003 Jan;125(1):178-83 [12539002.001]
  • [Cites] Crit Care Med. 2003 Feb;31(2):353-8 [12576936.001]
  • [Cites] Nat Rev Drug Discov. 2007 Aug;6(8):662-80 [17667957.001]
  • [Cites] Crit Care Med. 1999 Sep;27(9):1738-44 [10507592.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2005 Feb;288(2):H486-96 [15374823.001]
  • [Cites] Curr Med Chem. 2005;12(3):267-75 [15723618.001]
  • [Cites] Circulation. 2005 Mar 1;111(8):988-95 [15710754.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3483-8 [15728348.001]
  • [Cites] FASEB J. 2005 Mar;19(3):401-3 [15611153.001]
  • [Cites] Curr Drug Targets CNS Neurol Disord. 2005 Apr;4(2):179-94 [15857303.001]
  • [Cites] Nat Rev Drug Discov. 2005 May;4(5):421-40 [15864271.001]
  • [Cites] Pharmacol Res. 2005 Jul;52(1):15-24 [15911330.001]
  • [Cites] Neuropathol Appl Neurobiol. 2000 Feb;26(1):55-66 [10736067.001]
  • [Cites] Circ Res. 2000 Dec 8;87(12):1123-32 [11110769.001]
  • [Cites] Br J Pharmacol. 2001 Feb;132(4):815-27 [11181422.001]
  • [Cites] Trends Pharmacol Sci. 2005 Jun;26(6):302-10 [15925705.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Jul;314(1):53-60 [15784653.001]
  • [Cites] J Neurosci Res. 2005 Jul 15;81(2):190-8 [15931673.001]
  • [Cites] Cardiovasc Res. 2005 Aug 1;67(2):225-33 [16005301.001]
  • [Cites] Curr Vasc Pharmacol. 2005 Jul;3(3):221-9 [16026319.001]
  • [Cites] Curr Vasc Pharmacol. 2005 Jul;3(3):231-46 [16026320.001]
  • [Cites] Curr Vasc Pharmacol. 2005 Jul;3(3):267-83 [16026323.001]
  • [Cites] Curr Vasc Pharmacol. 2005 Jul;3(3):285-91 [16026324.001]
  • [Cites] Curr Vasc Pharmacol. 2005 Jul;3(3):293-9 [16026325.001]
  • [Cites] Lancet. 2005 Nov 12;366(9498):1711-7 [16291064.001]
  • [Cites] Antioxid Redox Signal. 2005 Nov-Dec;7(11-12):1568-80 [16356120.001]
  • [Cites] J Biol Chem. 2005 Dec 30;280(52):43121-30 [16207712.001]
  • [Cites] Transplant Proc. 2005 Nov;37(9):3684-7 [16386505.001]
  • [Cites] Hypertens Res. 2005 Oct;28(10):779-86 [16471171.001]
  • [Cites] Curr Opin Pharmacol. 2006 Apr;6(2):136-41 [16483848.001]
  • [Cites] Curr Opin Cell Biol. 2006 Apr;18(2):145-51 [16516457.001]
  • [Cites] Thromb Haemost. 2006 Jan;95(1):43-8 [16543960.001]
  • [Cites] Mol Med. 2006 Jul-Aug;12(7-8):143-52 [17088946.001]
  • [Cites] Mech Ageing Dev. 2007 Feb;128(2):173-81 [17116320.001]
  • [Cites] Dement Geriatr Cogn Disord. 2007;23(4):215-8 [17290104.001]
  • [Cites] Neuroscience. 2007 Apr 14;145(4):1267-72 [17084037.001]
  • [Cites] Curr Med Chem. 2007;14(11):1179-87 [17504138.001]
  • [Cites] Clin Exp Rheumatol. 2007 Mar-Apr;25(2):281-6 [17543154.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(9):1673-84 [17540609.001]
  • [Cites] Free Radic Biol Med. 2007 Sep 1;43(5):763-80 [17664140.001]
  • [Cites] Pharmacol Res. 2005 Jul;52(1):109-18 [15911339.001]
  • [Cites] Mol Cell Biochem. 2007 Sep;303(1-2):19-25 [17396231.001]
  • [Cites] Ann N Y Acad Sci. 2007 Aug;1109:338-44 [17785323.001]
  • [Cites] Eur J Cancer. 2007 Sep;43(14):2124-33 [17714938.001]
  • [Cites] Transplant Proc. 2007 Sep;39(7):2099-101 [17889105.001]
  • [Cites] Anticancer Agents Med Chem. 2007 Sep;7(5):515-23 [17896912.001]
  • [Cites] Apoptosis. 2007 Nov;12(11):2037-49 [17828454.001]
  • [Cites] Cardiovasc Drug Rev. 2007 Fall;25(3):235-60 [17919258.001]
  • [Cites] Mol Cell Biol. 2007 Nov;27(21):7475-85 [17785446.001]
  • [Cites] Front Biosci. 2008;13:3046-82 [17981777.001]
  • [Cites] Int J Mol Med. 2007 Dec;20(6):783-92 [17982684.001]
  • [Cites] Trends Pharmacol Sci. 2007 Nov;28(11):556-60 [17950909.001]
  • [Cites] Circulation. 2007 Nov 13;116(20):2315-24 [17967979.001]
  • [Cites] Curr Opin Investig Drugs. 2007 Dec;8(12):1051-6 [18058575.001]
  • (PMID = 18535182.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM060915; United States / Intramural NIH HHS / / Z01 AA000375-02; United States / Intramural NIH HHS / / Z99 AA999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oxidants; 14691-52-2 / Peroxynitrous Acid; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 130
  • [Other-IDs] NLM/ PMC2438280
  •  go-up   go-down


13. Kim SY, Gul R, Rah SY, Kim SH, Park SK, Im MJ, Kwon HJ, Kim UH: Molecular mechanism of ADP-ribosyl cyclase activation in angiotensin II signaling in murine mesangial cells. Am J Physiol Renal Physiol; 2008 Apr;294(4):F982-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • ADP-ribosyl cyclase (ADPR-cyclase) produces a Ca(2+)-mobilizing second messenger cyclic ADP-ribose (cADPR) from NAD(+).
  • Treatment of MMCs with ANG II induced an increase in intracellular Ca(2+) concentrations through a transient Ca(2+) release via an inositol 1,4,5-trisphosphate receptor and a sustained Ca(2+) influx via L-type Ca(2+) channels.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • 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 = 18272599.001).
  • [ISSN] 1931-857X
  • [Journal-full-title] American journal of physiology. Renal physiology
  • [ISO-abbreviation] Am. J. Physiol. Renal Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Pyridines; 0 / Vasoconstrictor Agents; 11128-99-7 / Angiotensin II; 119340-53-3 / Cyclic ADP-Ribose; 130663-39-7 / PD 123319; EC 3.2.2.5 / ADP-ribosyl Cyclase; SY7Q814VUP / Calcium
  •  go-up   go-down


1
Advertisement
4. Ogawa T, Ueda Y, Yoshimura K, Shigeoka S: Comprehensive analysis of cytosolic Nudix hydrolases in Arabidopsis thaliana. J Biol Chem; 2005 Jul 1;280(26):25277-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nudix hydrolases are a family of proteins that catalyze the hydrolysis of a variety of nucleoside diphosphate derivatives.
  • These findings suggest that most cytosolic AtNUDTs may substantially function in the sanitization of potentially hazardous ADP-ribose and the regulation of the cellular NADH/NAD(+) ratio in plant cells.
  • On the other hand, the AtNUDT1 protein had the ability to hydrolyze 8-oxo-dGTP with a K(m) value of 6.8 mum and completely suppress the increased frequency of spontaneous mutations in the Escherichia coli mutT(-) strain, indicating that AtNUDT1 is a functional homologue of E. coli MutT in A. thaliana and is involved in the prevention of spontaneous mutation.
  • [MeSH-minor] Adenosine Diphosphate Ribose / chemistry. Amino Acid Motifs. Amino Acid Sequence. Catalysis. Chloroplasts / metabolism. Chromatography, High Pressure Liquid. Deoxyguanine Nucleotides / chemistry. Electrophoresis, Polyacrylamide Gel. Escherichia coli / metabolism. Escherichia coli Proteins / chemistry. Genetic Complementation Test. Humans. Hydrolysis. Kinetics. Molecular Sequence Data. Multigene Family. Mutation. Phosphoric Monoester Hydrolases / chemistry. Plasmids / metabolism. Protein Binding. Recombinant Proteins / chemistry. Saccharomyces cerevisiae / metabolism. Sequence Homology, Amino Acid. Substrate Specificity

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • The Arabidopsis Information Resource. Linked Gene Data (subscription/membership/fee required).
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878881.001).
  • [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 / Arabidopsis Proteins; 0 / Deoxyguanine Nucleotides; 0 / Escherichia coli Proteins; 0 / Recombinant Proteins; 139307-94-1 / 8-oxodeoxyguanosine triphosphate; 20762-30-5 / Adenosine Diphosphate Ribose; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.6.1.- / NUDT1 protein, Arabidopsis; EC 3.6.1.- / Pyrophosphatases; EC 3.6.1.- / mutT protein, E coli; EC 3.6.1.9 / nucleotide pyrophosphatase
  •  go-up   go-down


15. Guttikonda SK, Trupti J, Bisht NC, Chen H, An YQ, Pandey S, Xu D, Yu O: Whole genome co-expression analysis of soybean cytochrome P450 genes identifies nodulation-specific P450 monooxygenases. BMC Plant Biol; 2010;10:243
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Cytochrome P450 monooxygenases (P450s) catalyze oxidation of various substrates using oxygen and NAD(P)H.
  • The recent availability of the soybean genome sequence allows us to identify and analyze soybean putative P450s at a genome scale.
  • The tissue-specific expression patterns of these P450 genes were analyzed and the expression of a representative set of genes were confirmed by qRT-PCR.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Plant Mol Biol. 2003 Dec;53(6):733-43 [15082922.001]
  • [Cites] Plant Physiol. 2003 Sep;133(1):63-72 [12970475.001]
  • [Cites] Pharmacogenetics. 1996 Feb;6(1):1-42 [8845856.001]
  • [Cites] Plant Mol Biol. 1996 May;31(2):323-35 [8756596.001]
  • [Cites] Drug Metabol Drug Interact. 1995;12(3-4):189-206 [8820852.001]
  • [Cites] Mol Gen Genet. 1998 May;258(4):315-22 [9648734.001]
  • [Cites] Plant Physiol. 1998 Aug;117(4):1393-400 [9701595.001]
  • [Cites] Arch Biochem Biophys. 1999 Sep 1;369(1):1-10 [10462435.001]
  • [Cites] J Am Chem Soc. 2005 Sep 14;127(36):12709-16 [16144421.001]
  • [Cites] Annu Rev Plant Biol. 2006;57:335-60 [16669765.001]
  • [Cites] Plant Physiol. 2006 May;141(1):121-34 [16531481.001]
  • [Cites] Methods Mol Biol. 2006;320:1-10 [16719369.001]
  • [Cites] Plant J. 2006 Oct;48(2):261-73 [17018035.001]
  • [Cites] Plant Cell Physiol. 2007 Mar;48(3):381-90 [17251202.001]
  • [Cites] Planta. 2007 Jun;226(1):109-23 [17273868.001]
  • [Cites] Nucleic Acids Res. 2007 Jul;35(Web Server issue):W678-82 [17483516.001]
  • [Cites] Mol Biol Evol. 2007 Aug;24(8):1596-9 [17488738.001]
  • [Cites] BMC Plant Biol. 2008;8:47 [18433503.001]
  • [Cites] Science. 2009 Sep 25;325(5948):1688-92 [19779199.001]
  • [Cites] Plant Physiol. 2009 Oct;151(2):574-89 [19700560.001]
  • [Cites] Plant Physiol. 2009 Nov;151(3):1167-74 [19605552.001]
  • [Cites] Phytochemistry. 2009 Dec;70(17-18):1940-7 [19818975.001]
  • [Cites] Nucleic Acids Res. 2010 Jan;38(Database issue):D211-22 [19920124.001]
  • [Cites] Nature. 2010 Jan 14;463(7278):178-83 [20075913.001]
  • [Cites] Plant Physiol. 2010 Feb;152(2):541-52 [19933387.001]
  • [Cites] Plant J. 2010 Jul 1;63(1):86-99 [20408999.001]
  • [Cites] BMC Plant Biol. 2010;10:160 [20687943.001]
  • [Cites] Plant Physiol. 1999 Nov;121(3):821-8 [10557230.001]
  • [Cites] Nat Biotechnol. 2000 Feb;18(2):208-12 [10657130.001]
  • [Cites] Mol Cell. 2000 Jan;5(1):121-31 [10678174.001]
  • [Cites] DNA Cell Biol. 2000 May;19(5):307-17 [10855798.001]
  • [Cites] FEBS Lett. 2000 Sep 15;481(2):183-8 [10996320.001]
  • [Cites] Trends Plant Sci. 2000 Mar;5(3):116-23 [10707077.001]
  • [Cites] Arch Biochem Biophys. 2001 Feb 15;386(2):281-9 [11368353.001]
  • [Cites] Cell. 2001 Jun 1;105(5):625-36 [11389832.001]
  • [Cites] Curr Opin Plant Biol. 2002 Jun;5(3):230-6 [11960741.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46051-8 [12351632.001]
  • [Cites] Adv Ther. 2003 Jan-Feb;20(1):50-78 [12772818.001]
  • [Cites] Genome Res. 2003 Sep;13(9):2129-41 [12952881.001]
  • [Cites] Plant Mol Biol. 2004 Mar;54(5):623-39 [15356384.001]
  • (PMID = 21062474.001).
  • [ISSN] 1471-2229
  • [Journal-full-title] BMC plant biology
  • [ISO-abbreviation] BMC Plant Biol.
  • [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] England
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Plant Proteins; 0 / Soybean Proteins; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.- / Mixed Function Oxygenases
  • [Other-IDs] NLM/ PMC3095325
  •  go-up   go-down


16. Massi G, Vellone VG, Pagliarello C, Fabrizi G: Plantar melanoma that mimics melanocytic nevi: a report of 4 cases with lymph node metastases and with review of positive and negative controls. Am J Dermatopathol; 2009 Apr;31(2):117-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plantar melanoma that mimics melanocytic nevi: a report of 4 cases with lymph node metastases and with review of positive and negative controls.
  • We report 4 cases of melanoma localized on the sole with some striking histological similarities to the compound nevi.
  • One case showed inguinal lymph node metastases after a diagnosis of compound nevus made 5 years earlier.
  • The other 3 cases were sent to us in consultation as suspected plantar lesions; a diagnosis of melanoma mimicking compound nevus was proposed: the sentinel lymph node technique was accordingly performed and resulted positive.
  • These 4 index cases were compared with 26 cases of ordinary plantar melanoma and with 117 cases of benign compound plantar nevi.
  • Histologically, the similarity of areas of these 4 cases of plantar melanoma to compound plantar nevi (namely Miescher, Clark, or acral lentiginous nevus) is so close that it may prove misleading in the diagnostic pathway.
  • In such cases, an erroneous diagnosis of benign lesion may be made.
  • The correct diagnosis of melanoma can, however, be done by combining the clinical and pathological findings.
  • In fact, this deceptive form of melanoma mimicking a compound nevus is characterized by patients' advanced age (>45 years), large lateral diameters (>10 mm), and significant depth of the lesion (>1 mm).
  • In our 4 cases, such features were combined with one or more of the following histological clues: lentiginous (ie, continuous) proliferation of enlarged and hyperchromatic melanocytes aligned in single units at the dermoepidermal junction; extensive eccrine duct melanocytic infiltration; dermal melanocytes with slight nuclear enlargement, nuclear membrane thickening and folding, and conspicuous central nucleoli; and cellular pleomorphism of the epidermal and dermal component.
  • In conclusion, a small group of plantar melanoma has striking similarities with compound nevi.
  • Only the correlation of clinical data (old age of the patient and large size of the lesion) with subtle architectural and cytological alterations (depth of the lesion, lentiginous melanocytic epidermal and eccrine proliferation, and cellular alteration and mitoses) allows a correct diagnosis.
  • [MeSH-major] Dermis / pathology. Melanoma / secondary. Nevus, Pigmented / pathology. Skin Neoplasms / 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
  • (PMID = 19318796.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Hong S, Brass A, Seman M, Haag F, Koch-Nolte F, Dubyak GR: Lipopolysaccharide, IFN-gamma, and IFN-beta induce expression of the thiol-sensitive ART2.1 Ecto-ADP-ribosyltransferase in murine macrophages. J Immunol; 2007 Nov 1;179(9):6215-27
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nicotinamide adenosine dinucleotide (NAD) can act as a modulator of multiple immune and inflammatory responses when released into extracellular compartments.
  • These actions of extracellular NAD are largely mediated by a family of mammalian ecto-ADP-ribosyltransferases (ARTs) that covalently modify target extracellular or cell surface proteins by transferring ADP-ribose to arginine or cysteine residues.
  • Collectively, these studies identify ART2.1 as a new candidate for linking autocrine/paracrine activation of inflammatory macrophages to the release of NAD, a critical intracellular metabolite.

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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 = 17947697.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM36387
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Sulfhydryl Compounds; 77238-31-4 / Interferon-beta; 82115-62-6 / Interferon-gamma; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / Art2a protein, mouse; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


18. Kurtasova LM, Golovanova AE, Savchenko AA: Enzymatic status of blood lymphocytes in young children with Epstein-Barr virus infection. Bull Exp Biol Med; 2010 Sep;149(3):337-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Activities of NAD(PH)-dependent dehydrogenases in peripheral blood lymphocytes were studied in children aged 1-3 years in the dynamics of the disease caused by Epstein-Barr virus.

  • MedlinePlus Health Information. consumer health - Infectious Mononucleosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21246096.001).
  • [ISSN] 1573-8221
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Immunoglobulin M; EC 1.6.- / NADH, NADPH Oxidoreductases
  •  go-up   go-down


19. Ding Y, Prieto VG, Zhang PS, Rosenthal S, Smith KJ, Skelton HG, Diwan AH: Nuclear expression of the antiapoptotic protein survivin in malignant melanoma. Cancer; 2006 Mar 1;106(5):1123-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, its diagnostic value in differentiating melanomas from nevi has not yet been examined.
  • METHODS: Tissue microarray blocks were constructed with paraffin-fixed tissue of 19 nevi, 18 dysplastic nevi, 24 malignant melanomas, and 31 metastatic melanomas.
  • Nuclear immunoreactivity for survivin (i.e., > or = 25% of cells exhibiting and/or at least moderately intense staining) was seen in a subset of melanomas but not in nevi or dysplastic nevi (P < 0.05).
  • These data may underscore the importance of nuclear survivin in progression to melanoma and may prove useful in the differential diagnosis of melanoma versus nevus.
  • [MeSH-major] Melanoma / genetics. Microtubule-Associated Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. Skin Neoplasms / genetics
  • [MeSH-minor] Cell Nucleus / chemistry. Cell Survival. Diagnosis, Differential. Disease Progression. Gene Expression Profiling. Humans. Inhibitor of Apoptosis Proteins. Nevus / diagnosis. Oligonucleotide Array Sequence Analysis

  • 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 = 16456815.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
  •  go-up   go-down


20. Reutter JC, Long EM, Morrell DS, Thomas NE, Groben PA: Eruptive post-chemotherapy in situ melanomas and dysplastic nevi. Pediatr Dermatol; 2007 Mar-Apr;24(2):135-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eruptive post-chemotherapy in situ melanomas and dysplastic nevi.
  • A 22-year-old white man without a personal or family history of atypical nevi had received chemotherapy for pre-B-cell acute lymphocytic leukemia at age 17 that included L-asparaginase, prednisone, methotrexate, mercaptopurine, daunorubicin, and cytoxan.
  • Upon examination, two dark, atypical appearing plaques with irregular borders and numerous pink papules of varying shapes and sizes were noted on his chest, back, and abdomen.
  • Histology of specimens of both types of lesions revealed three moderately atypical compound dysplastic melanocytic nevi and three in situ melanomas.
  • The lesions with only features of dysplastic nevi exhibited dermal fibrosis, cytologic atypia, junctional shoulders, lentiginous spread, and focal pigmentation.
  • The lesions with in situ melanomas in addition demonstrated pagetoid spread, extension down adnexal structures, and more severe cytologic atypia.
  • Malignant melanoma has been associated with chronic immunosuppression, and benign nevi have been reported to erupt after chemotherapy.
  • We report an occurrence of multiple eruptive dysplastic nevi and in situ melanomas appearing shortly after completion of chemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Drug Eruptions / etiology. Dysplastic Nevus Syndrome / chemically induced. Immunosuppressive Agents / adverse effects. Melanoma / chemically induced. Skin Neoplasms / chemically induced

  • 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 = 17461808.001).
  • [ISSN] 0736-8046
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
  •  go-up   go-down


21. Hammer H, Tóth-Molnár E, Oláh J, Dobozy A: [Connection between uveal melanoma and dysplastic naevus syndrome]. Magy Onkol; 2005;49(1):15-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Connection between uveal melanoma and dysplastic naevus syndrome].
  • [Transliterated title] Az uvealis melanoma és a dysplasticus naevus-syndroma kapcsolata.
  • The dysplastic naevus syndrome increases the risk of cutaneous (RR: 4.36; CI: 1.84-10.36) as well as uveal melanoma (RR: 4.22; CI: 1.81-9.84).
  • A significantly higher occurrence rate of conjunctival naevi (3.2% vs. 0%; p=0.029), choroidal naevi (5.2% vs. 0.7%; p=0.023) and iris freckles (17.1% vs. 5.6%; p=0.002) could be detected in the dysplastic naevus syndrome patients compared to subjects in the control group.
  • The presence of cutaneous dysplastic naevi in uveal melanoma patients increases the risk of the prognostically worse--epitheloid or mixed--forms of uveal melanoma (RR: 5.97%; CI: 1.61-22.14), compared to patients without cutaneous atypical naevi.
  • [MeSH-major] DNA, Neoplasm / analysis. Dysplastic Nevus Syndrome / genetics. Melanoma / genetics. Skin Neoplasms / genetics. Uveal Neoplasms / genetics


22. Kobilková J, Jirásek JE, Jedlicková J, Benešová O, Mašata J: [Prevention of the invasion of malignant cells of gynecologic tumors during surgery]. Ceska Gynekol; 2010 Dec;75(6):553-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • During gynecologic surgery of a choriocarcinoma and of an ovarian carcinoma Luksch and Cernoch prooved trace of malignant cells within the blood circulation related to the manipulation of tumors during surgery.
  • CONCLUSION: Although the members are small, there is doubt, that the ligation of oviducts and hypogastric vessels prior radical surgeries in patients affected by malignant gynecologic tumors substantially reduces metastazing of malignant cells nad improve the five years survival of surgically treated patients with gynecologic malignant tumors.


23. Medina M: Structural and mechanistic aspects of flavoproteins: photosynthetic electron transfer from photosystem I to NADP+. FEBS J; 2009 Aug;276(15):3942-58
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition to their role in photosynthesis, flavodoxin and ferredoxin-NADP(+) reductase are ubiquitous flavoenzymes that deliver NAD(P)H or low midpoint potential one-electron donors to redox-based metabolisms in plastids, mitochondria and bacteria.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19583765.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ferredoxins; 0 / Flavoproteins; 0 / Photosystem I Protein Complex; 53-59-8 / NADP
  • [Number-of-references] 155
  •  go-up   go-down


24. Hashimoto Y, Ookuma S, Nishida E: Lifespan extension by suppression of autophagy genes in Caenorhabditis elegans. Genes Cells; 2009 Jun;14(6):717-26
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Moreover, our analysis suggests that the lifespan extension, which is induced by RNAi of unc-51, bec-1 or atg-9 after development, does not require the transcription factor daf-16, the NAD(+)-dependent protein deacetylase sir-2.1 or the genes related to mitochondrial functions.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19469880.001).
  • [ISSN] 1365-2443
  • [Journal-full-title] Genes to cells : devoted to molecular & cellular mechanisms
  • [ISO-abbreviation] Genes Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Caenorhabditis elegans Proteins
  •  go-up   go-down


25. Merrell MD, Augustine LM, Slitt AL, Cherrington NJ: Induction of drug metabolism enzymes and transporters by oltipraz in rats. J Biochem Mol Toxicol; 2008 Mar-Apr;22(2):128-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, OPZ induced microsomal epoxide hydrolase, NAD(P)H quinone oxidoreductase, and Cyp3a1/23 equally in both genders, indicating a CAR-independent mechanism of induction of these genes.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2008 Wiley Periodicals, Inc.
  • (PMID = 18418891.001).
  • [ISSN] 1099-0461
  • [Journal-full-title] Journal of biochemical and molecular toxicology
  • [ISO-abbreviation] J. Biochem. Mol. Toxicol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / T32 ES007091; United States / NIEHS NIH HHS / ES / ES011646; United States / NIEHS NIH HHS / ES / F32 ES011239; United States / NIEHS NIH HHS / ES / F32 ES011239-01; United States / NIEHS NIH HHS / ES / ES006694; United States / NIDDK NIH HHS / DK / R01 DK068039; United States / NIEHS NIH HHS / ES / K22 ES011646; United States / NIEHS NIH HHS / ES / F32 ES011239-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Pharmaceutical Preparations; 0 / Pyrazines; 6N510JUL1Y / oltipraz; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, rat
  •  go-up   go-down


26. Yoon HY, Kang NI, Lee HK, Jang KY, Park JW, Park BH: Sulforaphane protects kidneys against ischemia-reperfusion injury through induction of the Nrf2-dependent phase 2 enzyme. Biochem Pharmacol; 2008 Jun 1;75(11):2214-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Phase 2 enzymes such as heme oxygenase-1, NAD(P)H: quinone oxidoreductase 1, glutathione reductase, and glutathione peroxidase participate in adaptive and protective responses to oxidative stress and various inflammatory stimuli.

  • Hazardous Substances Data Bank. OXYGEN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18407246.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isothiocyanates; 0 / NF-E2-Related Factor 2; 0 / Thiocyanates; 4478-93-7 / sulforafan; S88TT14065 / Oxygen
  •  go-up   go-down


27. Roldán MD, Pérez-Reinado E, Castillo F, Moreno-Vivián C: Reduction of polynitroaromatic compounds: the bacterial nitroreductases. FEMS Microbiol Rev; 2008 May;32(3):474-500
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bacterial nitroreductases are flavoenzymes that catalyze the NAD(P)H-dependent reduction of the nitro groups on nitroaromatic and nitroheterocyclic compounds.

  • BioCyc. gene/protein/disease-specific - nfsB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18355273.001).
  • [ISSN] 0168-6445
  • [Journal-full-title] FEMS microbiology reviews
  • [ISO-abbreviation] FEMS Microbiol. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Nitro Compounds; EC 1.7.- / Nitroreductases
  • [Number-of-references] 256
  •  go-up   go-down


28. Xiao Z, Xu P: Acetoin metabolism in bacteria. Crit Rev Microbiol; 2007 Apr-Jun;33(2):127-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The excretion of acetoin, which can be diagnosed by the Voges Proskauer test and serves as a microbial classification marker, has its vital physiological meanings to these microbes mainly including avoiding acification, participating in the regulation of NAD/NADH ratio, and storaging carbon.

  • Hazardous Substances Data Bank. ACETOIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17558661.001).
  • [ISSN] 1040-841X
  • [Journal-full-title] Critical reviews in microbiology
  • [ISO-abbreviation] Crit. Rev. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / catabolite control proteins, bacteria; BG4D34CO2H / Acetoin
  • [Number-of-references] 159
  •  go-up   go-down


29. Hishida A, Terakura S, Emi N, Yamamoto K, Murata M, Nishio K, Sekido Y, Niwa T, Hamajima N, Naoe T: GSTT1 and GSTM1 deletions, NQO1 C609T polymorphism and risk of chronic myelogenous leukemia in Japanese. Asian Pac J Cancer Prev; 2005 Jul-Sep;6(3):251-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We conducted a prevalent case-control study with 51 chronic myelogenous leukemia (CML) cases and 476 controls to investigate the associations between glutathione S-transferase T1 (GSTT1), glutathione S-transferase M1 (GSTM1) deletions, and the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism with risk of chronic myelocytic leukemia in Japanese.
  • Incidence case-control studies with a larger statistical power are now required to confirm our findings.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • 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 = 16235982.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
  •  go-up   go-down


30. Lindner HA, Nadeau G, Matte A, Michel G, Ménard R, Cygler M: Site-directed mutagenesis of the active site region in the quinate/shikimate 5-dehydrogenase YdiB of Escherichia coli. J Biol Chem; 2005 Feb 25;280(8):7162-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent YdiB and AroE crystal structures revealed the presence of a NAD(P)-binding and a catalytic domain.

  • BioCyc. gene/protein/disease-specific - ydiB .
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. L-Lysine .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15596430.001).
  • [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 / Escherichia coli Proteins; 058C04BGYI / Quinic Acid; 30KYC7MIAI / Aspartic Acid; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.25 / Shikimate dehydrogenase; K3Z4F929H6 / Lysine
  •  go-up   go-down


31. Fukushima T, Wada T, Ohtsu H, Tanaka K: Photoinduced four- and six-electron reduction of mononuclear ruthenium complexes having NAD+ analogous ligands. Dalton Trans; 2010 Dec 28;39(48):11526-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photoinduced four- and six-electron reduction of mononuclear ruthenium complexes having NAD+ analogous ligands.
  • The high efficiency photochemical two-, four- and six-electron reductions of [Ru(bpy)(2)(pbn)](2+) ([1](2+)), [2](2+) and [3](2+), respectively, by taking advantage of proton coupled two electron reduction of NAD(+) analogous type ligands such as pbn opens a general pathway for multi-electron reduction of metal complexes via illumination with visible light.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20830398.001).
  • [ISSN] 1477-9234
  • [Journal-full-title] Dalton transactions (Cambridge, England : 2003)
  • [ISO-abbreviation] Dalton Trans
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


32. Li M, Li Y, Chen J, Wei W, Pan X, Liu J, Liu Q, Leu W, Zhang L, Yang X, Lu J, Wang K: Copper ions inhibit S-adenosylhomocysteine hydrolase by causing dissociation of NAD+ cofactor. Biochemistry; 2007 Oct 16;46(41):11451-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Copper ions inhibit S-adenosylhomocysteine hydrolase by causing dissociation of NAD+ cofactor.
  • Binding of Cu2+ to SAHH resulted in the release of NAD+ cofactors, explaining the loss of the enzymatic activity of SAHH.
  • Further investigation by an ESR probe and computational simulation suggested that Cu2+ could bind at the central channel and interrupt the subunit interactions of SAHH, resulting in a large decrease in affinity to the NAD+ cofactor.
  • [MeSH-major] Adenosylhomocysteinase / antagonists & inhibitors. Adenosylhomocysteinase / chemistry. Copper / pharmacology. NAD / metabolism

  • Hazardous Substances Data Bank. COPPER, 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 = 17892301.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoenzymes; 0 / Recombinant Proteins; 0U46U6E8UK / NAD; 789U1901C5 / Copper; EC 3.3.1.1 / Adenosylhomocysteinase
  •  go-up   go-down


33. Petrova GV, Donchenko GV: [Cytotoxicity of troglitazone, structural analogue of alpha-tocopherol is mediated by inhibition of NAD(P)H:quinone oxidoreductase]. Ukr Biokhim Zh (1999); 2009 Jul-Aug;81(4):105-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cytotoxicity of troglitazone, structural analogue of alpha-tocopherol is mediated by inhibition of NAD(P)H:quinone oxidoreductase].
  • It is established, that alpha-tocopherol and pioglitazone in concentration up to 100 microM did not change the rat thymocytes viability while troglitazone and alpha-tocopherol with a short side chain up to 6 atoms of carbon (alpha-tocopherol C6) have the expressed cytotoxic effect.
  • This is the first report demonstrating that troglitazone and alpha-tocopherol C6, unlike a-tocopherol and pioglitazone substantially inhibited the activity of NAD(P)H:quinone oxidoreductase (DT-diaphorase) and this effect is increased with specific DT-diaphorase inhibitor, dicoumarol.
  • Based on these observations, we generalize that cytotoxic action of troglitazone and alpha-tocopherol C6 is connected with the presence in their structure of chroman ring with a lateral chain modified in relation to alpha-tocopherol and is mediated by inhibition of DT-diaphorase, a detoxifying enzyme of xenobiotics.
  • [MeSH-major] Chromans / pharmacology. NAD(P)H Dehydrogenase (Quinone) / antagonists & inhibitors. Thiazolidinediones / pharmacology. Thymus Gland / drug effects. alpha-Tocopherol / pharmacology

  • Hazardous Substances Data Bank. VITAMIN E .
  • Hazardous Substances Data Bank. DICUMAROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20387640.001).
  • [Journal-full-title] Ukraïnsʹkyĭ biokhimichnyĭ z︠h︡urnal (1999 )
  • [ISO-abbreviation] Ukr Biokhim Zh (1999)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Chromans; 0 / Enzyme Inhibitors; 0 / Thiazolidinediones; 7QID3E7BG7 / Dicumarol; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); H4N855PNZ1 / alpha-Tocopherol; I66ZZ0ZN0E / troglitazone
  •  go-up   go-down


34. Wang B, Jin F, Xie Y, Tang Y, Kan R, Zheng C, Yang Z, Wang L: Association analysis of NAD(P)H:quinone oxidoreductase gene 609 C/T polymorphism with Alzheimer's disease. Neurosci Lett; 2006 Dec 6;409(3):179-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association analysis of NAD(P)H:quinone oxidoreductase gene 609 C/T polymorphism with Alzheimer's disease.
  • Alterations of the NAD(P)H:quinone oxidoreductase (NQO1) activity are associated with Alzheimer's disease (AD).
  • A polymorphism consisting of a single nucleotide (C-->T) change at position 609 of NQO1 influences the NQO1 activity.
  • [MeSH-major] Alzheimer Disease / enzymology. Alzheimer Disease / epidemiology. Genetic Testing / methods. NAD(P)H Dehydrogenase (Quinone) / genetics. Risk Assessment / methods

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • MedlinePlus Health Information. consumer health - Genetic Testing.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17027152.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  •  go-up   go-down


35. Zhou M, Deng L, Wen D, Shang L, Jin L, Dong S: Highly ordered mesoporous carbons-based glucose/O2 biofuel cell. Biosens Bioelectron; 2009 May 15;24(9):2904-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OMCs are used as supports for both stably confining the electrocatalyst (i.e., meldola's blue, MDB) for NADH oxidation and the anodic biocatalyst (i.e., NAD(+)-dependent glucose dehydrogenase, GDH) for glucose oxidation, and for facilitating direct electrochemistry of the cathodic biocatalyst (i.e., laccase, LAC) for O(2) electroreduction.
  • In 0.10 M pH 6.0 PBS containing 20 mM NAD(+) and 60 mM glucose under the air-saturated atmosphere, the open circuit voltage (0.82 V) and the maximum power output (38.7 microW cm(-2) (at 0.54 V)) of the assembled compartment-less OMCs-based BFC are both higher than those of carbon nanotubes (CNTs)-based BFC (0.75 V and 2.1 microW cm(-2) (at 0.46 V)).
  • [MeSH-minor] Catalysis. Electrochemistry. Electrodes. Kinetics. NAD / chemistry. Oxazines / chemistry. Oxidation-Reduction. Porosity

  • Hazardous Substances Data Bank. GLUCOSE .
  • Hazardous Substances Data Bank. OXYGEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19321330.001).
  • [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] 0 / Nanotubes, Carbon; 0 / Oxazines; 0U46U6E8UK / NAD; 7057-57-0 / Meldola blue; EC 1.1.1.47 / Glucose 1-Dehydrogenase; IY9XDZ35W2 / Glucose; S88TT14065 / Oxygen
  •  go-up   go-down


76. Ma B, Pan SJ, Zupancic ML, Cormack BP: Assimilation of NAD(+) precursors in Candida glabrata. Mol Microbiol; 2007 Oct;66(1):14-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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 .
  • The Lens. Cited by Patents in .
  • [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


77. Dasgupta BR, Antharavally BS, Tepp W, Evenson ML: Botulinum neurotoxin types A, B, and E: fragmentations by autoproteolysis and other mechanisms including by O-phenanthroline-dithiothreitol, and association of the dinucleotides NAD(+)/NADH with the heavy chain of the three neurotoxins. Protein J; 2005 Aug;24(6):337-68
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Botulinum neurotoxin types A, B, and E: fragmentations by autoproteolysis and other mechanisms including by O-phenanthroline-dithiothreitol, and association of the dinucleotides NAD(+)/NADH with the heavy chain of the three neurotoxins.
  • The first evidence of autoproteolytic activity of the approximately 50-kDa light chain of the clostridial neurotoxins (NT) is traceable to the observations that the light chains of botulinum NT serotypes A and E, separated from their approximately 100-kDa heavy chain conjugate, were found cleaved at the amino side of Tyr250 and Arg244, respectively [DasGupta and Foley (1989).
  • None of the identified cleaved bonds (-P1-P1' -) in one serotype (except Asp-Pro) was found common in other serotypes or cleaved within itself at a second site.
  • After separation from the heavy chain self-cleavages of the light chains of type A, B and E at Tyr249-Tyr250, Gln258-Ser259 and Ile243-Arg244, respectively indicate an intriguing feature (in the aligned sequences these bonds of type A and B are 2 and type A and E are 4 peptide bonds apart) that may have some role in the NT's structure-function relationship yet to be understood.
  • We point out that autoproteolysis of a single peptide bond (Phe418-Thr419 or Phe422-Glu423) in NT type A reported by Ahmed et al. (2001) can potentially generate proteolytically active light chain freed of the heavy chain; this is an efficient pathway, that by-passes nicking by a trypsin-like protease(s) inside the intrachain disulfide bridge and its reductive cleavage.
  • The metal chelator O-phenanthroline (above critical miceller concentration) in the presence of dithiothreitol cleaved type E NT at limited sites generating discrete 114-, 87-, 49-, 42-, and 31-kDa fragments but degraded NTs type A and B extensively.
  • The dinucleotide NAD(+)/NADH associated with the NTs type A, B and E (2-3 NADH per protein molecule) via their H-chains, and a portion of the H-chain (toward the C-terminus) appears to exhibit limited amino acid sequence homology with lactate dehydrogenase-a representative NAD(+)/NADH binding protein.
  • [MeSH-minor] Amino Acid Sequence. Botulinum Toxins, Type A / metabolism. Dithiothreitol. L-Lactate Dehydrogenase / chemistry. Molecular Weight. NAD / metabolism. Peptide Hydrolases / metabolism. Phenanthrolines. Sequence Homology, Amino Acid

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Toxicon. 1983;21(4):535-45 [6353669.001]
  • [Cites] Nat Struct Biol. 1998 Oct;5(10):898-902 [9783750.001]
  • [Cites] J Mol Biol. 1999 Jul 2;290(1):37-48 [10388556.001]
  • [Cites] J Gen Microbiol. 1986 Jul;132(7):1981-8 [2432159.001]
  • [Cites] Biochem J. 1992 Jul 1;285 ( Pt 1):9-12 [1637325.001]
  • [Cites] J Biol Chem. 1996 Aug 2;271(31):18322-5 [8702470.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] Toxicon. 2001 Oct;39(10 ):1515-31 [11478959.001]
  • [Cites] FEBS Lett. 1996 May 20;386(2-3):133-6 [8647267.001]
  • [Cites] J Biol Chem. 1985 Sep 5;260(19):10461-6 [4030755.001]
  • [Cites] FEBS Lett. 1997 Jun 16;409(3):339-42 [9224685.001]
  • [Cites] J Biol Chem. 1992 Jul 25;267(21):14721-9 [1634516.001]
  • [Cites] Anal Biochem. 1989 Nov 15;183(1):108-21 [2619035.001]
  • [Cites] Nature. 1994 Dec 1;372(6505):415-6 [7984234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3208-13 [14982988.001]
  • [Cites] Biochem J. 1997 Mar 1;322 ( Pt 2):507-10 [9065770.001]
  • [Cites] J Mol Biol. 1999 Sep 3;291(5):1091-104 [10518945.001]
  • [Cites] Arch Biochem Biophys. 1984 Jul;232(1):172-8 [6430237.001]
  • [Cites] FEBS Lett. 1997 Nov 24;418(1-2):1-5 [9414082.001]
  • [Cites] Biochimie. 1989 Nov-Dec;71(11-12):1193-200 [2517479.001]
  • [Cites] J Physiol (Paris). 1990;84(3):220-8 [2074545.001]
  • [Cites] Methods Enzymol. 1985;117:346-54 [4079809.001]
  • [Cites] Toxicon. 1980;18(5-6):705-10 [7222076.001]
  • [Cites] J Protein Chem. 2001 Apr;20(3):221-31 [11565902.001]
  • [Cites] Nat Struct Biol. 2003 Jan;10(1):13-8 [12459720.001]
  • [Cites] Infect Immun. 2003 Mar;71(3):1147-54 [12595426.001]
  • [Cites] J Biol Chem. 1987 Feb 25;262(6):2660-3 [3029090.001]
  • [Cites] FASEB J. 1996 Sep;10(11):1257-69 [8836039.001]
  • [Cites] J Biol Chem. 1997 Feb 7;272(6):3459-64 [9013591.001]
  • [Cites] Eur J Biochem. 1992 Mar 1;204(2):657-67 [1541280.001]
  • [Cites] Arch Biochem Biophys. 1988 Oct;266(1):142-51 [3178218.001]
  • [Cites] Can J Microbiol. 1968 Jul;14(7):805-7 [4879302.001]
  • [Cites] Biochemistry. 2004 Mar 2;43(8):2209-16 [14979717.001]
  • [Cites] J Biol Chem. 1992 May 5;267(13):9053-8 [1577743.001]
  • [Cites] FEBS Lett. 1998 Jun 5;429(1):78-82 [9657387.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1992 Feb;345(2):227-34 [1570025.001]
  • [Cites] Infect Immun. 1989 Oct;57(10):3053-7 [2506129.001]
  • [Cites] Biochemistry. 2003 Nov 4;42(43):12539-49 [14580200.001]
  • [Cites] Biochemistry. 1998 Apr 14;37(15):5267-78 [9548758.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20353-8 [8702770.001]
  • [Cites] Toxicon. 2001 Feb-Mar;39(2-3):233-43 [10978741.001]
  • [Cites] J Neurochem. 1999 Jan;72 (1):327-37 [9886085.001]
  • [Cites] Protein Sci. 1999 Mar;8(3):518-28 [10091654.001]
  • [Cites] J Protein Chem. 1997 Oct;16(7):701-12 [9330228.001]
  • [Cites] J Cell Biol. 2003 Sep 29;162(7):1293-303 [14504267.001]
  • [Cites] J Protein Chem. 1998 Apr;17 (3):187-96 [9588942.001]
  • [Cites] J Protein Chem. 1998 Jul;17(5):417-28 [9717738.001]
  • [Cites] FEBS Lett. 2002 Dec 18;532(3):423-6 [12482605.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1316-21 [12552129.001]
  • [Cites] J Biol Chem. 1995 May 5;270(18):10566-70 [7737992.001]
  • [Cites] Toxicon. 1988;26(9):817-25 [3201486.001]
  • [Cites] J Biol Chem. 1987 Jul 25;262(21):10035-8 [3611052.001]
  • [Cites] Nat Struct Biol. 2000 Aug;7(8):693-9 [10932256.001]
  • [Cites] Clin Med (Lond). 2004 May-Jun;4(3):258-61 [15244362.001]
  • [Cites] Anal Biochem. 1986 Jul;156(1):213-9 [3740411.001]
  • [Cites] Biochimie. 2000 May;82(5):427-46 [10865130.001]
  • [Cites] Biochimie. 1990 Sep;72(9):661-4 [2126206.001]
  • [Cites] Toxicon. 1984;22(3):415-24 [6382680.001]
  • [Cites] Methods Enzymol. 1973;27:441-55 [4773289.001]
  • [Cites] Biochim Biophys Acta. 1962 Oct 8;63:530-2 [13955687.001]
  • (PMID = 16323041.001).
  • [ISSN] 1572-3887
  • [Journal-full-title] The protein journal
  • [ISO-abbreviation] Protein J.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS17742; United States / NINDS NIH HHS / NS / NS24545
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Peptide Fragments; 0 / Phenanthrolines; 0U46U6E8UK / NAD; 0Y70779M1F / rimabotulinumtoxinB; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.4.- / Peptide Hydrolases; EC 3.4.24.69 / Botulinum Toxins; EC 3.4.24.69 / Botulinum Toxins, Type A; T579M564JY / botulinum toxin type E; T8ID5YZU6Y / Dithiothreitol; W4X6ZO7939 / 1,10-phenanthroline
  •  go-up   go-down


78. Lukacik P, Keller B, Bunkoczi G, Kavanagh KL, Lee WH, Adamski J, Oppermann U: Structural and biochemical characterization of human orphan DHRS10 reveals a novel cytosolic enzyme with steroid dehydrogenase activity. Biochem J; 2007 Mar 15;402(3):419-27
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol.
  • Furthermore, the product of oestradiol oxidation, oestrone, was identified in intact cells transfected with a construct plasmid encoding the DHRS10 protein.
  • It also reveals a broad and deep active site cleft into which NAD+ and oestradiol can be docked in a catalytically competent orientation.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • SciCrunch. HGNC: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Endocrinol. 2001 Jan 22;171(1-2):137-49 [11165022.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):499-525 [11306071.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):699-705 [11306087.001]
  • [Cites] Curr Opin Chem Biol. 2001 Aug;5(4):375-82 [11470599.001]
  • [Cites] Eur J Biochem. 2001 Aug;268(15):4113-25 [11488903.001]
  • [Cites] Comb Chem High Throughput Screen. 2001 Nov;4(7):545-52 [11669066.001]
  • [Cites] Endocrinol Metab Clin North Am. 2002 Mar;31(1):63-78 [12055991.001]
  • [Cites] Sci STKE. 2002 Jun 25;2002(138):pe29 [12084905.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25677-84 [11976334.001]
  • [Cites] Eur J Neurosci. 2002 Aug;16(3):445-53 [12193187.001]
  • [Cites] Eur J Biochem. 2002 Sep;269(18):4409-17 [12230552.001]
  • [Cites] J Neurosci. 2002 Oct 1;22(19):8391-401 [12351713.001]
  • [Cites] J Neurochem. 2002 Nov;83(3):713-26 [12390533.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4984-90 [12414862.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):2030-5 [12397058.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D255-7 [14681406.001]
  • [Cites] Obes Res. 2004 Jan;12(1):9-17 [14742837.001]
  • [Cites] Recent Prog Horm Res. 2004;59:359-93 [14749510.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2004 Mar;60(Pt 3):432-8 [14993666.001]
  • [Cites] Synapse. 2000 Jan;35(1):39-44 [10579806.001]
  • [Cites] Hepatology. 2000 Apr;31(4):990-6 [10733557.001]
  • [Cites] Methods Enzymol. 2000;316:372-83 [10800688.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24333-40 [10811639.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2000 Aug;56(Pt 8):965-72 [10944333.001]
  • [Cites] Mol Cell Endocrinol. 2001 Jan 22;171(1-2):1-4 [11165003.001]
  • [Cites] Mol Cell Endocrinol. 2004 Apr 15;218(1-2):7-20 [15130507.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):2711-6 [15181046.001]
  • [Cites] Mol Neurobiol. 1988 Fall;2(3):183-200 [3077066.001]
  • [Cites] Rev Neurosci. 1994 Jan-Mar;5(1):27-41 [8019704.001]
  • [Cites] Biochem J. 1994 Dec 15;304 ( Pt 3):787-92 [7818482.001]
  • [Cites] Biochemistry. 1995 May 9;34(18):6003-13 [7742302.001]
  • [Cites] Biochem J. 1996 Mar 15;314 ( Pt 3):839-45 [8615778.001]
  • [Cites] Structure. 1996 Aug 15;4(8):905-15 [8805577.001]
  • [Cites] J Mol Biol. 1997 May 9;268(3):678-85 [9171291.001]
  • [Cites] Genomics. 1997 Nov 15;46(1):112-9 [9403065.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1319-24 [9543162.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] Anat Embryol (Berl). 1999 May;199(5):379-90 [10221449.001]
  • [Cites] Exp Gerontol. 2004 Nov-Dec;39(11-12):1579-86 [15582272.001]
  • [Cites] Semin Reprod Med. 2005 May;23(2):172-9 [15852203.001]
  • [Cites] Endocr Rev. 2005 May;26(3):308-12 [15851820.001]
  • [Cites] J Neurobiol. 2005 Jul;64(1):34-46 [15884004.001]
  • [Cites] Curr Neurovasc Res. 2005 Oct;2(4):287-301 [16181121.001]
  • [Cites] Mol Cell Endocrinol. 2006 Mar 27;248(1-2):61-71 [16414178.001]
  • [ErratumIn] Biochem J. 2007 May 1;403(3):615. Kavanagh, Kathryn [Kavanagh, Kathryn L]; Hwa, Lee Wen [corrected to Lee, Wen Hwa]
  • (PMID = 17067289.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0U46U6E8UK / NAD; EC 1.1.- / 17-Hydroxysteroid Dehydrogenases; EC 1.1.- / HSD17B14 protein, human
  • [Other-IDs] NLM/ PMC1863559
  •  go-up   go-down


79. Rey P, Lopez-Real A, Sanchez-Iglesias S, Muñoz A, Soto-Otero R, Labandeira-Garcia JL: Angiotensin type-1-receptor antagonists reduce 6-hydroxydopamine toxicity for dopaminergic neurons. Neurobiol Aging; 2007 Apr;28(4):555-67
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiotensin II activates (via type 1 receptors) NAD(P)H-dependent oxidases, which are a major source of superoxide, and is relevant in the pathogenesis of several cardiovascular diseases and certain degenerative changes associated with ageing.
  • Dopaminergic degeneration was also reduced by the NAD(P)H inhibitor apocynin.

  • Hazardous Substances Data Bank. DOPAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16621167.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic Agents; 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Naphthyridines; 0 / Thiobarbituric Acid Reactive Substances; 0 / ZD 7155; 8HW4YBZ748 / Oxidopamine; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; VTD58H1Z2X / Dopamine
  •  go-up   go-down


80. Dhawan AP, D'Alessandro B, Patwardhan S, Mullani N: Multispectral optical imaging of skin-lesions for detection of malignant melanomas. Conf Proc IEEE Eng Med Biol Soc; 2009;2009:5352-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multispectral optical imaging of skin-lesions for detection of malignant melanomas.
  • Optical imaging of skin-lesions for early detection and management of the most fatal skin-cancer malignant melanoma is of significant interest in mass screening of skin-lesions with high-risk population.
  • Surface illumination based optical imaging methods such as epiluminescence light microscopy (ELM) through "Dermascopy" has shown a significant potential in improving early diagnosis of malignant melanomas.
  • We have developed a novel optical imaging system, the Nevoscope, that uses multispectral transillumination as to provide images of skin-lesions showing sub-surface pigmentation as well as vascular architecture based blood volume information.
  • This paper presents multispectral Nevoscope transillumination method to compare and analyze ratiometric measurements to epiluminescence imaging for its ability to discriminate malignant melanomas from dysplastic nevi and other normal skin-lesions.
  • [MeSH-major] Melanoma / diagnosis. Skin Neoplasms / diagnosis. Transillumination / instrumentation. Transillumination / methods

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19964673.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


81. Sorrentino SA, Bahlmann FH, Besler C, Müller M, Schulz S, Kirchhoff N, Doerries C, Horváth T, Limbourg A, Limbourg F, Fliser D, Haller H, Drexler H, Landmesser U: Oxidant stress impairs in vivo reendothelialization capacity of endothelial progenitor cells from patients with type 2 diabetes mellitus: restoration by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone. Circulation; 2007 Jul 10;116(2):163-73
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Small-interfering RNA silencing of NAD(P)H oxidase subunit p47(phox) reduced superoxide production and restored NO bioavailability and in vivo reendothelialization capacity of EPCs from diabetic patients.
  • Importantly, rosiglitazone therapy normalized NAD(P)H oxidase activity, restored NO bioavailability, and improved in vivo reendothelialization capacity of EPCs from diabetic patients (reendothelialized area: placebo versus rosiglitazone, 8+/-1% versus 38+/-5%; P<0.001).
  • CONCLUSIONS: In vivo reendothelialization capacity of EPCs derived from individuals with diabetes mellitus is severely impaired at least partially as a result of increased NAD(P)H oxidase-dependent superoxide production and subsequently reduced NO bioavailability.
  • Rosiglitazone therapy reduces NAD(P)H oxidase activity and improves reendothelialization capacity of EPCs from diabetic individuals, representing a potential novel mechanism whereby peroxisome proliferator-activated receptor-gamma agonism promotes vascular repair.


82. Izzicupo P, Di Valerio V, D' Amico MA, Di Mauro M, Pennelli A, Falone S, Alberti G, Amicarelli F, Miscia S, Gallina S, Di Baldassarre A: NAD(P)H oxidase and pro-inflammatory response during maximal exercise: role of C242T polymorphism of the P22PHOX subunit. Int J Immunopathol Pharmacol; 2010 Jan-Mar;23(1):203-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD(P)H oxidase and pro-inflammatory response during maximal exercise: role of C242T polymorphism of the P22PHOX subunit.
  • Intense exercise induces a pro-inflammatory status through a mechanism involving the NAD(P)H oxidase system.
  • We focused our attention on p22phox, a subunit of the NAD(P)H oxidase, and on its allelic polymorphism C242T, which is known to affect the functional activity of the enzyme.
  • In addition, the presence of T allele was associated with a higher cardiopulmonary efficiency as evidenced by a significantly lower Heart Rate (HR) at the peak of exercise and, when a dominant model was assumed, by a higher maximal oxygen uptake (VO2 max).
  • These results contribute to support the hypothesis of a systemic effect for the C242T polymorphism and of its possible functional rebound in healthy subjects.

  • MedlinePlus Health Information. consumer health - Exercise and Physical Fitness.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20378006.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; EC 1.11.1.7 / Peroxidase; EC 1.6.3.1 / CYBA protein, human; EC 1.6.3.1 / NADPH Oxidase; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


83. Chen R, Chen JY, Zhou LW: Metabolic patterns (NAD(P)H) in rat basophilic leukemia (RBL-2H3) cells and human hepatocellular carcinoma (Hep G2) cells with autofluorescence imaging. Ultrastruct Pathol; 2008 Sep-Oct;32(5):193-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolic patterns (NAD(P)H) in rat basophilic leukemia (RBL-2H3) cells and human hepatocellular carcinoma (Hep G2) cells with autofluorescence imaging.
  • Although the spatial and temporal distributions of cellular NAD(P)H concentrations have been theoretically predicted as typical patterns of the metabolism in living cells, so far such a pattern was observed only in neutrophils.
  • In this work, the dynamic NAD(P)H distributions in rat basophilic leukemia (RBL-2H3) and human hepatocellular carcinoma (Hep G2) cells were studied by imaging the autofluorescence of cellular NAD(P)H with a sensitive CCD detector in a confocal microscope.
  • The typical pattern of the cytoplasmic NAD(P)H wave traveling along the long axis of the elongated cell with a velocity of 2.2+/-0.6 mircom/s was detected in RBL-2H3 cells.
  • While in the case of Hep G2 cells, only the oscillation of the mitochondrial NAD(P)H was observed because the NAD(P)H mainly localized in mitochondria of Hep G2 cells.
  • These results confirm the metabolic pattern of NAD(P)H in living cells and suggest that the expression of the metabolic pattern probably differs in different cell lines.

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18958792.001).
  • [ISSN] 1521-0758
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 53-59-8 / NADP
  •  go-up   go-down


84. Horenstein AL, Sizzano F, Lusso R, Besso FG, Ferrero E, Deaglio S, Corno F, Malavasi F: CD38 and CD157 ectoenzymes mark cell subsets in the human corneal limbus. Mol Med; 2009 Mar-Apr;15(3-4):76-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.
  • The presence of enzymatically active NAD(+)-consumers in intact corneal cells was analyzed by high performance liquid chromatography (HPLC)-based assays.
  • The results of the work indicates that the human cornea is equipped with molecular tools capable of consuming extracellular NAD(+), and that CD157 is a potential marker of corneal limbal cells in the stem cell niche.
  • [MeSH-minor] Biomarkers / metabolism. Cornea / anatomy & histology. Cornea / metabolism. GPI-Linked Proteins. Humans. NAD / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Ophthalmol. 2004 Sep;88(9):1154-8 [15317707.001]
  • [Cites] Stem Cells. 2004;22(3):355-66 [15153612.001]
  • [Cites] Cell. 1989 Apr 21;57(2):201-9 [2702690.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1993 May;34(6):1983-90 [7684031.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1993 Aug;34(9):2672-9 [8344790.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Nov 15;196(3):1459-65 [8250903.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5325-9 [8202488.001]
  • [Cites] J Immunol. 1994 Aug 1;153(3):952-9 [7913116.001]
  • [Cites] J Biol Chem. 1994 Dec 2;269(48):30260-7 [7982936.001]
  • [Cites] FEBS Lett. 1994 Dec 19;356(2-3):244-8 [7805847.001]
  • [Cites] J Immunol. 1996 Jan 15;156(2):727-34 [8543826.001]
  • [Cites] J Biol Chem. 1996 Jul 5;271(27):15922-7 [8663150.001]
  • [Cites] Int Immunol. 1996 Nov;8(11):1643-50 [8943558.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Apr 28;233(3):801-5 [9168937.001]
  • [Cites] Protein Expr Purif. 1998 Feb;12(1):133-7 [9473467.001]
  • [Cites] Biochem J. 1998 Mar 15;330 ( Pt 3):1129-35 [9494077.001]
  • [Cites] Brain Res. 1999 Mar 6;821(1):17-25 [10064783.001]
  • [Cites] J Cell Biol. 1999 May 17;145(4):769-82 [10330405.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jun;46(6):1957-65 [15914609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9523-8 [15983386.001]
  • [Cites] Methods Mol Biol. 2005;308:191-208 [16082036.001]
  • [Cites] Clin Experiment Ophthalmol. 2006 Jan-Feb;34(1):64-73 [16451261.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Oct;47(10):4295-301 [17003418.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Nov;47(11):5032-8 [17065524.001]
  • [Cites] Semin Cell Dev Biol. 2006 Dec;17(6):654-66 [17178241.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Mar;48(3):978-84 [17325135.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):317-23 [17380198.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):334-41 [17380201.001]
  • [Cites] Antioxid Redox Signal. 2008 Feb;10(2):179-206 [18020963.001]
  • [Cites] Physiol Rev. 2008 Jul;88(3):841-86 [18626062.001]
  • [Cites] FASEB J. 2001 Jan;15(1):10-12 [11099492.001]
  • [Cites] Tissue Antigens. 2000 Dec;56(6):539-47 [11169244.001]
  • [Cites] Diabetes. 2001 May;50(5):985-91 [11334442.001]
  • [Cites] Glia. 2002 Sep;39(3):314-9 [12203397.001]
  • [Cites] Cell Biochem Funct. 2002 Dec;20(4):309-22 [12415565.001]
  • [Cites] Eur J Biochem. 2004 Mar;271(5):1025-34 [15009214.001]
  • [Cites] Cell. 2004 Mar 19;116(6):769-78 [15035980.001]
  • [Cites] Exp Eye Res. 2004 Mar;78(3):433-46 [15106923.001]
  • [Cites] Hum Immunol. 1984 Jan;9(1):9-20 [6693298.001]
  • (PMID = 19052657.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Grant] Italy / Telethon / / GTF06004
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / GPI-Linked Proteins; 0U46U6E8UK / NAD; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / ADP-ribosyl cyclase 2; EC 3.2.2.5 / Antigens, CD38
  •  go-up   go-down


85. Slominska EM, Yuen A, Osman L, Gebicki J, Yacoub MH, Smolenski RT: Cytoprotective effects of nicotinamide derivatives in endothelial cells. Nucleosides Nucleotides Nucleic Acids; 2008 Jun;27(6):863-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoprotective effects of nicotinamide derivatives in endothelial cells.
  • Following discovery of NAD(+)-dependent reactions that control gene expression, cytoprotection, and longevity, there has been a renewed therapeutic interest in precursors, such as nicotinamide and its derivatives.
  • We tested 20 analogues of nicotinamide for their ability to protect endothelial cells from peroxynitrite stress and their effect on poly (ADP-ribose) polymerase (PARP) activity.
  • Several nicotinamide derivatives protected endothelial cells from peroxynitrite-induced depletion of cellular NAD(+) and ATP concentrations, but only some of these compounds inhibited PARP.
  • We conclude that some nicotinamide derivatives provide protection of endothelial cells against peroxynitrite-induced injury independent of inhibition of PARP activity.
  • Preservation of the NAD(+) pool was a common effect of these compounds.
  • [MeSH-minor] Cell Line. Humans. NAD / metabolism. Poly(ADP-ribose) Polymerase Inhibitors. Time Factors

  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18600553.001).
  • [ISSN] 1532-2335
  • [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 / Poly(ADP-ribose) Polymerase Inhibitors; 0U46U6E8UK / NAD; 25X51I8RD4 / Niacinamide
  •  go-up   go-down


86. Bychkov PV, Shekhovtsova TN, Milaeva ER: Inhibition of horse liver alcohol dehydrogenase by methyltin compounds. Bioinorg Chem Appl; 2005;:191-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Data acquired on NAD-dependent ADH from horse liver and those regarding NAD-dependent LDH from sturgeon liver were compared.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18365099.001).
  • [ISSN] 1565-3633
  • [Journal-full-title] Bioinorganic chemistry and applications
  • [ISO-abbreviation] Bioinorg Chem Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2267099
  • [Keywords] NOTNLM ; NAD / alcohol dehydrogenase / inhibition type / methyltin compounds
  •  go-up   go-down


87. Brimfield AA, Novak MJ, Hodgson E: Thiodiglycol, the hydrolysis product of sulfur mustard: analysis of in vitro biotransformation by mammalian alcohol dehydrogenases using nuclear magnetic resonance. Toxicol Appl Pharmacol; 2006 Jun 15;213(3):207-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The intermediate nature of this mixture was determined spectrophotometrically when it was shown to drive the production of NADH when added to ADH and NAD.

  • Hazardous Substances Data Bank. THIODIGLYCOL .
  • Hazardous Substances Data Bank. BIS(2-CHLOROETHYL)SULFIDE .
  • 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 = 16417912.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Sulfhydryl Compounds; 9BW5T43J04 / 2,2'-thiodiethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; T8KEC9FH9P / Mustard Gas
  •  go-up   go-down


88. Lebe B, Pabuççuoglu U, Ozer E: Expression pattern of type IV collagen in sporadic dysplastic melanocytic nevi. Anal Quant Cytol Histol; 2008 Oct;30(5):291-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression pattern of type IV collagen in sporadic dysplastic melanocytic nevi.
  • OBJECTIVE: To investigate the expression and distribution pattern of type IV collagen in dysplastic nevi (DN) and to determine whether DN exhibits a morphologic difference from common melanocytic nevi (CMN) and cutaneous malignant melanomas (MM) and therefore can be classified as a separate entity.
  • STUDY DESIGN: We examined 33 DN specimens, 18 CMN specimens, and 10 MM specimens.
  • Twenty-one of 33 DN showed a continuous pattern of type IV collagen surrounding junctional nests in a concentric fashion while a discontinuous immunostaining pattern was observed in remaining cases.
  • The expression pattern of type IV collagen in DN was statistically different from CMN and MM.
  • CONCLUSION: Our results suggest sporadic DN is biologically different from CMN in terms of the capacity to synthesize type IV collagen, demonstrating that DN is not only morphologically but also biologically a different entity from CMN.

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18980161.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Collagen Type IV
  •  go-up   go-down


89. Barranco WT, Kim DH, Stella SL Jr, Eckhert CD: Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. Cell Biol Toxicol; 2009 Aug;25(4):309-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this paper, we report that boric acid (BA) inhibits NAD+ and NADP+ as well as mechanically induced release of stored Ca2+ in growing DU-145 prostate cancer cells.
  • NAD+-induced Ca2+ transients were partly inhibited at 250 microM BA and completely at 1,000 microM BA, whereas both NADP+ and mechanically induced transients were inhibited by 1,000 microM BA.
  • In vitro mass spectrometry analysis showed that BA formed adducts with the CD38 products and Ca2+ channel agonists cyclic adenosine diphosphate ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).
  • The BA analog, methylboronic acid (MBA; 250 and 1,000 microM), did not inhibit cell proliferation or NAD+, NADP+, or mechanically stimulated Ca2+ store release.
  • [MeSH-minor] Antigens, CD38 / metabolism. Calcium Signaling / drug effects. Cell Line, Tumor. Cyclic ADP-Ribose / metabolism. Humans. Male. NAD / metabolism. NADP / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • COS Scholar Universe. author profiles.
  • 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 = 18516691.001).
  • [ISSN] 1573-6822
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Boric Acids; 0U46U6E8UK / NAD; 119340-53-3 / Cyclic ADP-Ribose; 53-59-8 / NADP; EC 3.2.2.5 / Antigens, CD38; R57ZHV85D4 / boric acid; SY7Q814VUP / Calcium
  •  go-up   go-down


90. Casalino E, Calzaretti G, Landriscina M, Sblano C, Fabiano A, Landriscina C: The Nrf2 transcription factor contributes to the induction of alpha-class GST isoenzymes in liver of acute cadmium or manganese intoxicated rats: comparison with the toxic effect on NAD(P)H:quinone reductase. Toxicology; 2007 Jul 31;237(1-3):24-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Nrf2 transcription factor contributes to the induction of alpha-class GST isoenzymes in liver of acute cadmium or manganese intoxicated rats: comparison with the toxic effect on NAD(P)H:quinone reductase.
  • The stimulation is associated with a higher level of alpha-class GST proteins, whose induction is blocked by actinomycin D co-administration.
  • For comparison, we have evaluated the status of another important antioxidant enzyme, NAD(P)H:quinone reductase, 24h after cadmium or manganese administration.
  • [MeSH-major] Cadmium Chloride / toxicity. Chlorides / toxicity. Glutathione Transferase / biosynthesis. Isoenzymes / biosynthesis. Liver. NAD(P)H Dehydrogenase (Quinone) / biosynthesis. NF-E2 Transcription Factor, p45 Subunit / physiology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MANGANESE COMPOUNDS .
  • Hazardous Substances Data Bank. CADMIUM CHLORIDE .
  • Hazardous Substances Data Bank. MANGANESE CHLORIDE .
  • Hazardous Substances Data Bank. SELENIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17573173.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chlorides; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Manganese Compounds; 0 / NF-E2 Transcription Factor, p45 Subunit; 99Z2744345 / Ditiocarb; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, rat; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase alpha; H6241UJ22B / Selenium; J6K4F9V3BA / Cadmium Chloride; QQE170PANO / manganese chloride
  •  go-up   go-down


91. Diani-Moore S, Ram P, Li X, Mondal P, Youn DY, Sauve AA, Rifkind AB: Identification of the aryl hydrocarbon receptor target gene TiPARP as a mediator of suppression of hepatic gluconeogenesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin and of nicotinamide as a corrective agent for this effect. J Biol Chem; 2010 Dec 10;285(50):38801-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of the aryl hydrocarbon receptor target gene TiPARP as a mediator of suppression of hepatic gluconeogenesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin and of nicotinamide as a corrective agent for this effect.
  • TCDD suppressed hepatic glucose production, expression of key gluconeogenic genes, phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (G6Pase), and NAD(+) levels, and increased PARP activity and TiPARP expression.
  • TiPARP overexpression reproduced TCDD effects on glucose output and NAD(+) levels whereas TiPARP silencing diminished them.
  • The vitamin B3 constituent, nicotinamide (NAM), prevented TCDD suppression of glucose output, NAD(+), and gluconeogenic genes and stabilized PGC1α.
  • The corrective effects of NAM could be attributed to increased NAD(+) levels and suppression of AHR target gene induction.

  • Hazardous Substances Data Bank. GLUCOSE .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neuromolecular Med. 2009;11(1):28-42 [19288225.001]
  • [Cites] Mol Cell Biol. 2008 Jan;28(1):30-9 [17954562.001]
  • [Cites] Endocr Rev. 2010 Apr;31(2):194-223 [20007326.001]
  • [Cites] Oncogene. 2010 Aug 19;29(33):4617-24 [20531298.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2000;40:519-61 [10836146.001]
  • [Cites] Nature. 2001 Sep 13;413(6852):131-8 [11557972.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Nov 30;289(2):499-506 [11716501.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Arch Biochem Biophys. 2002 Aug 15;404(2):309-16 [12147270.001]
  • [Cites] Chem Biol Interact. 2002 Sep 20;141(1-2):131-60 [12213389.001]
  • [Cites] Hum Gene Ther. 2002 Sep 1;13(13):1561-70 [12228011.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):1843-55 [12612060.001]
  • [Cites] Biochemistry. 2003 Aug 12;42(31):9249-56 [12899610.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1982;22:517-54 [6282188.001]
  • [Cites] Toxicol Lett. 1985 Jun;25(3):247-58 [4012802.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Feb 14;174(3):1267-71 [1996990.001]
  • [Cites] Toxicology. 1991 Feb;66(2):133-44 [1849669.001]
  • [Cites] Arch Toxicol Suppl. 1992;15:151-5 [1510582.001]
  • [Cites] Toxicology. 1993 Mar 30;79(1):81-95 [8475501.001]
  • [Cites] Mol Pharmacol. 1993 Dec;44(6):1142-51 [8264550.001]
  • [Cites] Arch Toxicol. 1994;69(2):73-8 [7717864.001]
  • [Cites] Toxicol Appl Pharmacol. 1996 Sep;140(1):173-9 [8806883.001]
  • [Cites] J Biol Chem. 1996 Dec 20;271(51):33054-9 [8955152.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50754-63 [15381699.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1329-35 [15531890.001]
  • [Cites] Nature. 2005 Mar 3;434(7029):113-8 [15744310.001]
  • [Cites] Cell Metab. 2005 Jun;1(6):361-70 [16054085.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(24):10684-94 [16314495.001]
  • [Cites] Mol Pharmacol. 2006 Jan;69(1):140-53 [16214954.001]
  • [Cites] Toxicol Sci. 2006 Mar;90(1):96-110 [16330490.001]
  • [Cites] Drug Metab Rev. 2006;38(1-2):291-335 [16684662.001]
  • [Cites] Annu Rev Biochem. 2006;75:435-65 [16756498.001]
  • [Cites] J Biol Chem. 2006 Jul 14;281(28):19000-8 [16670093.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982.001]
  • [Cites] J Biochem Mol Toxicol. 2006;20(4):151-8 [16906519.001]
  • [Cites] Toxicol Appl Pharmacol. 2006 Dec 15;217(3):363-74 [17109908.001]
  • [Cites] J Med Chem. 2007 Dec 27;50(26):6458-61 [18052316.001]
  • [Cites] Chem Res Toxicol. 2008 Jan;21(1):102-16 [18076143.001]
  • [Cites] Toxicol Appl Pharmacol. 2009 Jan 1;234(1):1-13 [18948129.001]
  • [Cites] Anal Biochem. 2009 Feb 15;385(2):377-9 [19027704.001]
  • [Cites] AAPS J. 2006;8(4):E632-43 [17233528.001]
  • [Cites] Curr Opin Gastroenterol. 2007 Mar;23(2):164-70 [17268245.001]
  • [Cites] Nature. 2007 Mar 29;446(7135):562-6 [17392787.001]
  • [Cites] Toxicol Sci. 2007 Jul;98(1):5-38 [17569696.001]
  • [Cites] Toxicol Lett. 2007 Aug10;172(3):146-58 [17669606.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jul 7;106(27):11288-93 [19549853.001]
  • (PMID = 20876576.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA062948; United States / NCI NIH HHS / CA / T32-CA062948; United States / NIDDK NIH HHS / DK / R01-DK73466; United States / NIEHS NIH HHS / ES / R01 ES003606; United States / NIEHS NIH HHS / ES / R01-ES03606; United States / NIDDK NIH HHS / DK / R01 DK073466; United States / NCI NIH HHS / CB / N02-CB-666000
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Aryl Hydrocarbon; 0 / Transcription Factors; 0U46U6E8UK / NAD; 25X51I8RD4 / Niacinamide; 9005-79-2 / Glycogen; DO80M48B6O / Tetrachlorodibenzodioxin; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.5.1.- / SIRT1 protein, human; EC 3.5.1.- / Sirtuin 1; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2998137
  •  go-up   go-down


92. Wojnowski W, Obrebowski A, Pruszewicz A, Demenko G, Wiskirska-Woźnica B, Swidziński P: [Further research on speech tests]. Otolaryngol Pol; 2007;61(6):979-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Dalsze badania nad testami mowy utrudnionej.
  • [MeSH-major] Audiometry, Speech. Hearing Disorders / diagnosis. Noise

  • MedlinePlus Health Information. consumer health - Hearing Disorders and Deafness.
  • MedlinePlus Health Information. consumer health - Noise.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18546946.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


93. Chan KM, Rajab NF, Siegel D, Din LB, Ross D, Inayat-Hussain SH: Goniothalamin induces coronary artery smooth muscle cells apoptosis: the p53-dependent caspase-2 activation pathway. Toxicol Sci; 2010 Aug;116(2):533-48
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, the p53 elevation in GN-treated CASMCs was independent of NAD(P)H: quinone oxidoreductase 1 and Mdm-2 expression.
  • [MeSH-minor] Adenosine Triphosphate / analysis. Amino Acid Chloromethyl Ketones / pharmacology. Cells, Cultured. Cytochromes c / secretion. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Hydrogen Peroxide / metabolism. Membrane Potential, Mitochondrial / drug effects. NAD(P)H Dehydrogenase (Quinone) / metabolism. Oxygen Consumption / drug effects. Superoxides / metabolism

  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20498002.001).
  • [ISSN] 1096-0929
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Pyrones; 0 / Tumor Suppressor Protein p53; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 11062-77-4 / Superoxides; 34W9GO6B2Z / goniothalamin; 8L70Q75FXE / Adenosine Triphosphate; 9007-43-6 / Cytochromes c; BBX060AN9V / Hydrogen Peroxide; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 3.4.22.- / Caspase 2
  •  go-up   go-down


94. Xiao T, Shoeb M, Siddiqui MS, Zhang M, Ramana KV, Srivastava SK, Vasiliou V, Ansari NH: Molecular cloning and oxidative modification of human lens ALDH1A1: implication in impaired detoxification of lipid aldehydes. J Toxicol Environ Health A; 2009;72(9):577-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purified recombinant human lens ALDH1A1 exhibited optimal catalytic activity at pH 8 and preferred NAD(+) as cofactor and specifically catalyzed the oxidation of toxic lipid aldehydes such as 4-hydroxynonenal (HNE; K(m) = 4.8 microM) and malonaldehyde (K(m) MDA = 3.5 microM).
  • Further, modification of recombinant human lens ALDH1A1 with nitric oxide donors such as S-nitroso-N-acetylpenicillamine (SNAP) and S-nitrosoglutathione (GSNO) significantly inhibited the enzyme activity.

  • MedlinePlus Health Information. consumer health - Cataract.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochim Biophys Acta. 1980 Nov 7;620(2):281-96 [6254573.001]
  • [Cites] Mol Aspects Med. 2003 Aug-Oct;24(4-5):167-75 [12892994.001]
  • [Cites] Genome Res. 1996 Sep;6(9):791-806 [8889548.001]
  • [Cites] Enzyme. 1991;45(4):188-93 [1823864.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Jun;44(6):2675-82 [12766072.001]
  • [Cites] Eur J Biochem. 1999 Jun;262(3):704-12 [10411631.001]
  • [Cites] Biochem Mol Med. 1996 Jun;58(1):25-30 [8809342.001]
  • [Cites] J Biochem. 2000 Nov;128(5):771-6 [11056389.001]
  • [Cites] Biochem Pharmacol. 1991 Jun 1;41(11):1583-7 [2043148.001]
  • [Cites] Arch Ophthalmol. 2005 Aug;123(8):1102-5 [16087845.001]
  • [Cites] Biochem J. 2003 Dec 15;376(Pt 3):615-23 [12943535.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):261-73 [11306050.001]
  • [Cites] Free Radic Biol Med. 1991;11(1):81-128 [1937131.001]
  • [Cites] Pharmacogenetics. 1999 Aug;9(4):421-34 [10780262.001]
  • [Cites] Biochem Pharmacol. 1998 Jun 15;55(12 ):2007-15 [9714321.001]
  • [Cites] Biochim Biophys Acta. 1996 Dec 6;1291(3):182-8 [8980630.001]
  • [Cites] Mol Aspects Med. 2003 Aug-Oct;24(4-5):149-59 [12892992.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):57-69 [11306031.001]
  • [Cites] Structure. 1998 Dec 15;6(12):1541-51 [9862807.001]
  • [Cites] Bull World Health Organ. 2004 Nov;82(11):844-51 [15640920.001]
  • [Cites] DNA Cell Biol. 2003 May;22(5):329-38 [12941160.001]
  • [Cites] Biochem Pharmacol. 1985 Apr 15;34(8):1197-204 [3994742.001]
  • [Cites] Ophthalmologica. 2001 Mar-Apr;215(2):113-6 [11244341.001]
  • [Cites] Biochemistry. 1997 Dec 16;36(50):15801-9 [9398310.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3771-5 [2987944.001]
  • [Cites] Biochemistry. 1997 Nov 4;36(44):13748-54 [9354647.001]
  • [Cites] J Biol Chem. 1984 Oct 10;259(19):11986-90 [6480593.001]
  • [Cites] J Biol Chem. 2007 Aug 31;282(35):25668-76 [17567582.001]
  • [Cites] Alcohol Clin Exp Res. 1993 Aug;17(4):828-31 [8214422.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jan;46(1):259-67 [15623782.001]
  • [Cites] Lens Eye Toxic Res. 1990;7(2):161-71 [2275929.001]
  • [Cites] Arch Ophthalmol. 1993 Aug;111(8):1041-9 [8352686.001]
  • [Cites] FASEB J. 1995 Sep;9(12):1173-82 [7672510.001]
  • [Cites] FASEB J. 2003 Mar;17(3):417-25 [12631581.001]
  • [Cites] Semin Cell Dev Biol. 2008 Apr;19(2):100-12 [18077195.001]
  • [Cites] Curr Eye Res. 2001 Oct;23(4):307-11 [11852433.001]
  • [Cites] J Exp Zool. 1998 Sep-Oct 1;282(1-2):12-7 [9723161.001]
  • [Cites] J Cataract Refract Surg. 2002 Mar;28(3):507-12 [11973099.001]
  • [Cites] Gene. 1997 Jun 3;191(2):167-72 [9218716.001]
  • [Cites] Biochem J. 1978 Sep 1;173(3):787-98 [30447.001]
  • [Cites] Free Radic Biol Med. 2000 Oct 1;29(7):642-51 [11033416.001]
  • (PMID = 19296407.001).
  • [ISSN] 1528-7394
  • [Journal-full-title] Journal of toxicology and environmental health. Part A
  • [ISO-abbreviation] J. Toxicol. Environ. Health Part A
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R29 EY011490; United States / NEI NIH HHS / EY / R01 EY013014; United States / NEI NIH HHS / EY / EY13014; United States / NEI NIH HHS / EY / R01 EY011490; United States / NEI NIH HHS / EY / EY11490; United States / NIDDK NIH HHS / DK / R37 DK036118
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; EC 1.2.1.3 / ALDH1A1 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  •  go-up   go-down


95. Rathbone CR, Booth FW, Lees SJ: Sirt1 increases skeletal muscle precursor cell proliferation. Eur J Cell Biol; 2009 Jan;88(1):35-44
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Over-expression of the NAD+-dependent histone deacetylase Sirt1 increased MPC proliferation and cell cycle progression as evidenced by increased 5-bromo-2'-deoxyuridine (BrdU) incorporation, an increase in cell number, proliferating cell nuclear antigen expression, and the phosphorylation of retinoblastoma protein.
  • Using O2 levels as a platform to modulate basal Sirt1 protein, activation of Sirt1 activity with resveratrol in 20% O2 increased MPC proliferation while inhibition of Sirt1 with nicotinamide in 5% O2 lowered proliferation.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. OXYGEN .
  • 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] Mol Cell. 2003 Jul;12(1):51-62 [12887892.001]
  • [Cites] Science. 2003 Nov 28;302(5650):1575-7 [14645852.001]
  • [Cites] Science. 2004 Mar 26;303(5666):2011-5 [14976264.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10042-7 [15220471.001]
  • [Cites] Cell Prolif. 2004 Aug;37(4):267-77 [15245563.001]
  • [Cites] Exp Cell Res. 1986 Sep;166(1):209-19 [2874992.001]
  • [Cites] Cell. 1992 Oct 30;71(3):505-14 [1358458.001]
  • [Cites] Cell Prolif. 2008 Apr;41(2):193-207 [18336467.001]
  • [Cites] Dev Biol. 1994 Aug;164(2):588-603 [7913900.001]
  • [Cites] Cell. 1995 May 5;81(3):323-30 [7736585.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):574-8 [7911228.001]
  • [Cites] EMBO J. 1996 Dec 16;15(24):7060-9 [9003781.001]
  • [Cites] Genes Dev. 1997 Apr 1;11(7):847-62 [9106657.001]
  • [Cites] Methods Cell Biol. 1997;52:155-76 [9379949.001]
  • [Cites] Ann N Y Acad Sci. 1998 Nov 20;854:78-91 [9928422.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):760-4 [15716955.001]
  • [Cites] J Biol Chem. 2005 Apr 1;280(13):12339-43 [15713665.001]
  • [Cites] Am J Physiol Cell Physiol. 2006 Feb;290(2):C609-15 [16192302.001]
  • [Cites] Interdiscip Top Gerontol. 2007;35:137-58 [17063037.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E151-7 [16926381.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6823-32 [17197703.001]
  • [Cites] Biochem J. 2007 May 15;404(1):1-13 [17447894.001]
  • [Cites] Clin Nutr. 2007 Aug;26(4):389-99 [17499396.001]
  • [Cites] Ann Med. 2007;39(5):335-45 [17701476.001]
  • [Cites] Cell. 2001 Oct 19;107(2):149-59 [11672523.001]
  • [Cites] Cell. 2001 Oct 19;107(2):137-48 [11672522.001]
  • [Cites] Acta Physiol Scand. 1999 Dec;167(4):301-5 [10632630.001]
  • [Cites] J Mol Med (Berl). 2003 Jun;81(6):355-62 [12732930.001]
  • [Cites] J Gerontol A Biol Sci Med Sci. 2002 Oct;57(10):B359-65 [12242311.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 Oct;283(4):C1182-95 [12225982.001]
  • [Cites] Biochem Mol Biol Int. 1995 May;36(1):59-66 [7545052.001]
  • (PMID = 18922599.001).
  • [ISSN] 1618-1298
  • [Journal-full-title] European journal of cell biology
  • [ISO-abbreviation] Eur. J. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG018780; United States / NIA NIH HHS / AG / AG18780; United States / NIAMS NIH HHS / AR / AR048523; United States / NIAMS NIH HHS / AR / T32 AR048523-05; None / None / / R01 AG018780-08; United States / NIAMS NIH HHS / AR / T32 AR048523; United States / NIA NIH HHS / AG / R01 AG018780-08; United States / NIAMS NIH HHS / AR / AR048523-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cyclin-Dependent Kinase Inhibitor p21; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.5.1.- / Sirt1 protein, mouse; EC 3.5.1.- / Sirt1 protein, rat; EC 3.5.1.- / Sirtuin 1; EC 3.5.1.- / Sirtuins; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ NIHMS88690; NLM/ PMC2656762
  •  go-up   go-down


96. Lantsman Y, Tan KS, Morada M, Yarlett N: Biochemical characterization of a mitochondrial-like organelle from Blastocystis sp. subtype 7. Microbiology; 2008 Sep;154(Pt 9):2757-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biochemical characterization of a mitochondrial-like organelle from Blastocystis sp. subtype 7.
  • Biochemical characterization enabled the demonstration of several key enzymes that allowed the construction of a metabolic pathway consisting of an incomplete Krebs cycle linked to the oxygen-sensitive enzymes pyruvate : NADP(+) oxidoreductase (PNO), acetate : succinate CoA transferase (ASCT) and succinate thiokinase (STK), which cumulatively are responsible for recycling CoA and generating ATP.
  • The organelle differs from typical aerobic mitochondria in possessing an oxygen-sensitive PNO that can use FAD(+) or FMN(+) as electron acceptor but is inactive with NAD(+), Spinacia oleracea ferredoxin or Clostridium pasteurianum ferredoxin.
  • A second cluster with 56 % sequence similarity to the pyruvate : ferredoxin oxidoreductase (PFOR) from Trichomonas vaginalis was also identified, which is in agreement with the concept that the PNO gene arose through the fusion of a eubacterial gene for PFOR with the gene for NADPH : cytochrome p450 reductase.
  • Based upon the results of this study, the Blastocystis organelle falls into the category of a MLO.
  • [MeSH-minor] Adenosine Triphosphate / biosynthesis. Animals. Citric Acid Cycle. Coenzyme A-Transferases / metabolism. Flavin Mononucleotide / metabolism. Flavin-Adenine Dinucleotide / metabolism. Ketone Oxidoreductases / metabolism. NAD / metabolism. Protozoan Proteins / metabolism. Succinate-CoA Ligases / metabolism

  • COS Scholar Universe. author profiles.
  • 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).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18757809.001).
  • [ISSN] 1350-0872
  • [Journal-full-title] Microbiology (Reading, England)
  • [ISO-abbreviation] Microbiology (Reading, Engl.)
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / NCDDG AI40320
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protozoan Proteins; 0U46U6E8UK / NAD; 146-14-5 / Flavin-Adenine Dinucleotide; 7N464URE7E / Flavin Mononucleotide; 8L70Q75FXE / Adenosine Triphosphate; EC 1.2.- / Ketone Oxidoreductases; EC 1.2.1.51 / pyruvate dehydrogenase (NADP+); EC 2.8.3.- / Coenzyme A-Transferases; EC 2.8.3.- / acetate-succinate CoA-transferase; EC 6.2.1.- / Succinate-CoA Ligases
  •  go-up   go-down


97. Deganuto M, Pittis MG, Pines A, Dominissini S, Kelley MR, Garcia R, Quadrifoglio F, Bembi B, Tell G: Altered intracellular redox status in Gaucher disease fibroblasts and impairment of adaptive response against oxidative stress. J Cell Physiol; 2007 Jul;212(1):223-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gaucher disease (GD) is a lysosomal storage disorder, due to glucosylceramide (GlcCer) accumulation in several body tissues, which causes cellular failure by yet unidentified mechanisms.
  • The ROS rise is probably due to NAD(P)H oxidase activity, being inhibited by the treatment with diphenylene iodonium chloride.


98. de la Lastra CA, Villegas I, Sánchez-Fidalgo S: Poly(ADP-ribose) polymerase inhibitors: new pharmacological functions and potential clinical implications. Curr Pharm Des; 2007;13(9):933-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Poly(ADP-ribose) polymerase (PARP) comprise of a family of enzymes which catalyses poly(ADP-ribosyl)ation of DNA-binding proteins.
  • PARP-1, the best characterised member, works as a DNA damage nick-sensor protein that uses beta-NAD(+) to form polymers of ADP-ribose and has been implicated in DNA repair, maintenance of genomic integrity and mammalian longevity.
  • The generation of free radicals, reactive oxygen species, and peroxynitrite causes overactivation of PARP resulting in the depletion of NAD(+) and ATP and consequently in necrotic cell death and organ dysfunction.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17430191.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Hypoglycemic Agents; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Protective Agents; 0 / Protein Subunits; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 375
  •  go-up   go-down


99. Grasberger H, De Deken X, Miot F, Pohlenz J, Refetoff S: Missense mutations of dual oxidase 2 (DUOX2) implicated in congenital hypothyroidism have impaired trafficking in cells reconstituted with DUOX2 maturation factor. Mol Endocrinol; 2007 Jun;21(6):1408-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dual oxidase 2 (DUOX2), a reduced NAD phosphate:O2 oxidoreductase flavoprotein, is a component of the thyrocyte H2O2 generator required for hormone synthesis at the apical plasma membrane.
  • D506N displays a partial deficiency phenotype with reduced surface expression of a mutant protein with normal intrinsic activity in generating H2O2.
  • DUOXA2 may thus be part of a secondary quality control system specific for DUOX2.

  • Genetic Alliance. consumer health - Congenital Hypothyroidism.
  • COS Scholar Universe. author profiles.
  • 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).
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17374849.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK15070; United States / NIDDK NIH HHS / DK / DK20595; United States / NCRR NIH HHS / RR / RR00055
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DUOXA2 protein, human; 0 / DUOXA2 protein, rat; 0 / Flavoproteins; 0 / Membrane Proteins; 0 / Polysaccharides; BBX060AN9V / Hydrogen Peroxide; EC 1.6.3.1 / DUOX2 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 3.2.1.96 / Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase
  •  go-up   go-down


100. Arita M, Oh SF, Chonan T, Hong S, Elangovan S, Sun YP, Uddin J, Petasis NA, Serhan CN: Metabolic inactivation of resolvin E1 and stabilization of its anti-inflammatory actions. J Biol Chem; 2006 Aug 11;281(32):22847-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • With NAD+ as a cofactor, recombinant 15-hydroxyprostaglandin dehydrogenase acted as an 18-hydroxyl dehydrogenase to form 18-oxo-RvE1.
  • At a concentration where RvE1 potently reduced polymorphonuclear leukocyte (PMN) recruitment in zymosan-induced peritonitis, 18-oxo-RvE1 was devoid of activity.
  • These results established the structure of a novel RvE1 initial metabolite, indicating that conversion of RvE1 to the oxo product represents a mode of RvE1 inactivation.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16757471.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-074448; United States / NIDCR NIH HHS / DE / P50-DE-016191
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid; 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Recombinant Proteins; AAN7QOV9EA / Eicosapentaenoic Acid; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.141 / 15-hydroxyprostaglandin dehydrogenase
  •  go-up   go-down






Advertisement