[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 1507
1. Mameza MG, Lockard JM, Zamora E, Hillefors M, Lavina ZS, Kaplan BB: Characterization of the adaptor protein ARH expression in the brain and ARH molecular interactions. J Neurochem; 2007 Nov;103(3):927-41
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.
  • A yeast two hybrid screen for ARH protein interactions in mouse brain identified the following binders: amyloid precursor-like protein 1, low density lipoprotein receptor-related protein (LRP) 1, LRP8, and GABA receptor-associated protein-like 1.
  • [MeSH-minor] Animals. Axons / metabolism. Axons / ultrastructure. Cell Line. Cytoskeletal Proteins / metabolism. Decapodiformes / genetics. Decapodiformes / metabolism. Evolution, Molecular. Ganglia, Sympathetic / metabolism. Ganglia, Sympathetic / ultrastructure. Humans. Membrane Proteins / metabolism. Mice. Molecular Sequence Data. Protein Binding / physiology. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, LDL / metabolism. Sequence Homology, Amino Acid. Tumor Suppressor Proteins / metabolism


2. Fluhrer R, Grammer G, Israel L, Condron MM, Haffner C, Friedmann E, Böhland C, Imhof A, Martoglio B, Teplow DB, Haass C: A gamma-secretase-like intramembrane cleavage of TNFalpha by the GxGD aspartyl protease SPPL2b. Nat Cell Biol; 2006 Aug;8(8):894-6
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.
  • We demonstrate that SPPL2b utilizes multiple intramembrane cleavages to liberate the intracellular domain of tumor necrosis factor alpha (TNFalpha) into the cytosol and the carboxy-terminal counterpart into the extracellular space.
  • [MeSH-major] Aspartic Acid Endopeptidases / metabolism. Endopeptidases / metabolism. Intracellular Membranes / metabolism. Tumor Necrosis Factor-alpha / metabolism. Zebrafish Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Amyloid Precursor Protein Secretases. Binding Sites / genetics. Cell Line. Cytosol / chemistry. Cytosol / enzymology. Cytosol / metabolism. Humans. Molecular Sequence Data. Mutation / genetics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization


3. Nakamura T, Higashi S, Tomoda K, Tsukano M, Baba S: Efficacy of etanercept in patients with AA amyloidosis secondary to rheumatoid arthritis. Clin Exp Rheumatol; 2007 Jul-Aug;25(4):518-22
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.
  • OBJECTIVE: The efficacy of biological therapies in rheumatoid arthritis (RA) is well known, but their hypothetical benefit in amyloid A (AA) amyloidosis secondary to RA still remains to be considered.
  • We evaluated the efficacy and safety of etanercept in serum amyloid A (SAA) 1.3 allele Japanese patients with AA amyloidosis secondary to RA.
  • [MeSH-major] Amyloidosis / drug therapy. Amyloidosis / etiology. Arthritis, Rheumatoid / complications. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use


Advertisement
4. Atkins CM, Oliva AA Jr, Alonso OF, Pearse DD, Bramlett HM, Dietrich WD: Modulation of the cAMP signaling pathway after traumatic brain injury. Exp Neurol; 2007 Nov;208(1):145-58
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.
  • Traumatic axonal injury, characterized by beta-amyloid precursor protein deposits in the external capsule, was also significantly reduced in rolipram-treated animals.
  • Furthermore, levels of the pro-inflammatory cytokines, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), were significantly decreased with rolipram treatment.

  • 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] J Biol Chem. 2003 Nov 14;278(46):45994-8 [12947093.001]
  • [Cites] J Neurosurg Anesthesiol. 2004 Jan;16(1):87-94 [14676577.001]
  • [Cites] Arthritis Res Ther. 2003;5(6):R317-28 [14680506.001]
  • [Cites] Biochem Pharmacol. 1985 Aug 15;34(16):2997-3000 [2992527.001]
  • [Cites] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756.001]
  • [Cites] J Neurochem. 1992 Oct;59(4):1581-4 [1328527.001]
  • [Cites] J Neuroimmunol. 1993 Feb;42(2):177-85 [8429103.001]
  • [Cites] Brain Res. 1993 Oct 8;624(1-2):94-102 [8252419.001]
  • [Cites] J Biol Chem. 1994 Apr 22;269(16):12190-5 [8163524.001]
  • [Cites] J Neurochem. 1994 Jul;63(1):266-70 [8207432.001]
  • [Cites] J Cereb Blood Flow Metab. 1994 Jul;14(4):615-9 [8014208.001]
  • [Cites] J Immunol. 1994 Jul 15;153(2):712-23 [8021507.001]
  • [Cites] Genes Dev. 1994 Nov 1;8(21):2527-39 [7958915.001]
  • [Cites] J Neurotrauma. 1994 Jun;11(3):289-301 [7996583.001]
  • [Cites] J Neurotrauma. 1994 Aug;11(4):357-68 [7837277.001]
  • [Cites] Int J Immunopharmacol. 1994 Oct;16(10):805-16 [7843852.001]
  • [Cites] J Neurosci. 1995 Mar;15(3 Pt 1):2030-9 [7891150.001]
  • [Cites] J Pharmacol Exp Ther. 1995 Mar;272(3):1313-20 [7891349.001]
  • [Cites] Eur J Pharmacol. 1995 Jan 5;272(1):107-10 [7713141.001]
  • [Cites] Nature. 1995 Apr 13;374(6523):647-50 [7715705.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3601-5 [7536938.001]
  • [Cites] Oncogene. 1995 Jul 6;11(1):97-106 [7624137.001]
  • [Cites] Arch Biochem Biophys. 1995 Sep 10;322(1):1-13 [7574662.001]
  • [Cites] J Neurosci. 1995 Dec;15(12):8223-33 [8613756.001]
  • [Cites] Brain Res Mol Brain Res. 1996 Mar;36(2):287-91 [8965649.001]
  • [Cites] J Neurotrauma. 1995 Dec;12(6):1035-43 [8742132.001]
  • [Cites] J Neurosci Res. 1996 Apr 15;44(2):157-64 [8723224.001]
  • [Cites] Science. 1996 Aug 16;273(5277):959-63 [8688081.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20828-35 [8702838.001]
  • [Cites] Acta Neurochir Suppl. 2000;76:207-12 [11450008.001]
  • [Cites] Brain Res Mol Brain Res. 2001 Aug 15;92(1-2):98-106 [11483246.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Aug;2(8):599-609 [11483993.001]
  • [Cites] J Cereb Blood Flow Metab. 2001 Oct;21(10):1189-98 [11598496.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Nov;299(2):753-9 [11602691.001]
  • [Cites] Neuropharmacology. 2002 Feb;42(2):262-9 [11804623.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2002 Apr;365(4):284-9 [11919652.001]
  • [Cites] Br J Pharmacol. 2002 Apr;135(7):1783-93 [11934820.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7628-33 [12032334.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):195-203; discussion 203 [12182417.001]
  • [Cites] J Neurotrauma. 2002 Aug;19(8):939-51 [12225654.001]
  • [Cites] Eur J Biochem. 2002 Sep;269(18):4559-65 [12230568.001]
  • [Cites] Exp Neurol. 2003 Dec;184(2):1017-26 [14769396.001]
  • [Cites] Inflamm Res. 2004 Jan;53(1):31-7 [15021978.001]
  • [Cites] Neuroscience. 2004;125(1):129-39 [15051152.001]
  • [Cites] Nat Med. 2004 Jun;10(6):610-6 [15156204.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 8;101(23):8786-90 [15173585.001]
  • [Cites] Mol Cell Neurosci. 2004 Jul;26(3):470-80 [15234351.001]
  • [Cites] Brain Res. 2004 Aug 6;1016(2):154-62 [15246851.001]
  • [Cites] Neurosurgery. 2004 Aug;55(2):416-24; discussion 424-5 [15271250.001]
  • [Cites] Behav Brain Res. 2004 Sep 23;154(1):99-106 [15302115.001]
  • [Cites] J Neurotrauma. 2004 Jul;21(7):842-53 [15307897.001]
  • [Cites] Acta Neurochir Suppl. 2004;89:69-74 [15335103.001]
  • [Cites] Neuroscience. 2004;128(2):305-22 [15350643.001]
  • [Cites] J Cereb Blood Flow Metab. 2004 Aug;24(8):934-43 [15362724.001]
  • [Cites] Glia. 2004 Nov 15;48(3):241-9 [15390118.001]
  • [Cites] Brain Res. 1980 Oct 27;200(1):93-103 [6251946.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35920-31 [12114522.001]
  • [Cites] Curr Opin Crit Care. 2002 Apr;8(2):101-5 [12386508.001]
  • [Cites] Biochem J. 2003 Feb 15;370(Pt 1):1-18 [12444918.001]
  • [Cites] J Neurotrauma. 2002 Dec;19(12):1555-67 [12542857.001]
  • [Cites] J Neural Transm (Vienna). 2003 Apr;110(4):363-72 [12658364.001]
  • [Cites] Trends Pharmacol Sci. 1996 Aug;17(8):294-8 [8810876.001]
  • [Cites] EMBO J. 1996 Sep 2;15(17):4629-42 [8887554.001]
  • [Cites] Eur J Pharmacol. 1997 Mar 5;321(3):273-8 [9085037.001]
  • [Cites] Neurochem Int. 1997 Apr-May;30(4-5):427-31 [9106257.001]
  • [Cites] Cell Signal. 1997 May-Jun;9(3-4):227-36 [9218122.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Oct;56(10):1132-41 [9329457.001]
  • [Cites] Brain Res Mol Brain Res. 1997 Sep;48(2):401-6 [9332737.001]
  • [Cites] Brain Res. 1997 Sep 12;768(1-2):177-84 [9369314.001]
  • [Cites] Neuroreport. 1997 Dec 1;8(17):3829-32 [9427378.001]
  • [Cites] Am J Respir Crit Care Med. 1998 Feb;157(2):351-70 [9476844.001]
  • [Cites] J Neurotrauma. 1998 Mar;15(3):163-70 [9528916.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4426-41 [9687510.001]
  • [Cites] Clin Neuropharmacol. 1998 Jul-Aug;21(4):236-44 [9704165.001]
  • [Cites] Mol Cell Biol. 1998 Oct;18(10):5678-89 [9742085.001]
  • [Cites] J Pharmacol Exp Ther. 1998 Nov;287(2):705-11 [9808700.001]
  • [Cites] Brain Res. 1998 Nov 23;812(1-2):97-104 [9813261.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):15020-5 [9844008.001]
  • [Cites] J Cereb Blood Flow Metab. 1999 Oct;19(10):1118-25 [10532636.001]
  • [Cites] J Neuroimmunol. 2000 Jun 1;105(1):20-30 [10713360.001]
  • [Cites] Annu Rev Biochem. 1999;68:821-61 [10872467.001]
  • [Cites] Eur J Med Chem. 2000 May;35(5):463-80 [10889326.001]
  • [Cites] Brain Res. 2001 Jan 12;888(2):275-286 [11150485.001]
  • [Cites] Neurosci Lett. 2001 Feb 2;298(2):103-6 [11163288.001]
  • [Cites] Glia. 2001 Mar 15;33(4):324-33 [11246231.001]
  • [Cites] Nature. 1998 Dec 3;396(6710):474-7 [9853756.001]
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):34594-602 [9852131.001]
  • [Cites] J Neurochem. 1999 Feb;72(2):565-75 [9930728.001]
  • [Cites] Neuroscience. 1999 Mar;89(2):437-52 [10077326.001]
  • [Cites] J Neuroimmunol. 1999 Jun 1;97(1-2):119-28 [10408965.001]
  • [Cites] J Neurotrauma. 1999 Jun;16(6):471-86 [10391364.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8721-6 [10411942.001]
  • [Cites] Ann Neurol. 2004 Nov;56(5):611-23 [15470752.001]
  • [Cites] J Clin Invest. 2004 Dec;114(11):1624-34 [15578094.001]
  • [Cites] Med Res Rev. 2005 Mar;25(2):229-44 [15514991.001]
  • [Cites] J Neurotrauma. 2005 Jan;22(1):42-75 [15665602.001]
  • [Cites] J Cereb Blood Flow Metab. 2005 Feb;25(2):234-46 [15647742.001]
  • [Cites] Neuroscience. 2005;133(1):1-15 [15893627.001]
  • [Cites] J Cereb Blood Flow Metab. 2006 Dec;26(12):1507-18 [16570077.001]
  • [Cites] Neurobiol Dis. 2007 Feb;25(2):266-73 [17184995.001]
  • [Cites] J Cereb Blood Flow Metab. 2007 May;27(5):939-49 [16955078.001]
  • [Cites] Stroke. 2007 May;38(5):1597-605 [17379823.001]
  • [Cites] Cell Calcium. 2003 Oct-Nov;34(4-5):425-30 [12909086.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Oct;307(1):246-53 [12954819.001]
  • [Cites] J Neurotrauma. 2003 Oct;20(10):929-41 [14588110.001]
  • (PMID = 17916353.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS042133-05; United States / NINDS NIH HHS / NS / NS042133-05; United States / NINDS NIH HHS / NS / NS42133; United States / NINDS NIH HHS / NS / NS30291; United States / NINDS NIH HHS / NS / NS056072-01A1; United States / NINDS NIH HHS / NS / R01 NS042133; United States / NINDS NIH HHS / NS / P50 NS030291-15; United States / NINDS NIH HHS / NS / R01 NS056072; United States / NINDS NIH HHS / NS / NS030291-15; United States / NINDS NIH HHS / NS / P50 NS030291; United States / NINDS NIH HHS / NS / R01 NS056072-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Interleukin-1beta; 0 / Phosphodiesterase 4 Inhibitors; 0 / Phosphodiesterase Inhibitors; 0 / Tumor Necrosis Factor-alpha; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K676NL63N7 / Rolipram
  • [Other-IDs] NLM/ NIHMS34649; NLM/ PMC2141537
  •  go-up   go-down


5. Velez-Pardo C, Del Rio MJ: Avoidance of Abeta[(25-35)] / (H(2)O(2)) -induced apoptosis in lymphocytes by the cannabinoid agonists CP55,940 and JWH-015 via receptor-independent and PI3K-dependent mechanisms: role of NF-kappaB and p53. Med Chem; 2006 Sep;2(5):471-9
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.
  • [MeSH-major] Amyloid beta-Peptides / pharmacology. Apoptosis / drug effects. Cannabinoids / agonists. Hydrogen Peroxide / pharmacology. Lymphocytes / drug effects. NF-kappa B / metabolism. Peptide Fragments / pharmacology. Phosphatidylinositol 3-Kinases / metabolism. Tumor Suppressor Protein p53 / metabolism

  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 17017986.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cannabinoids; 0 / Cyclohexanes; 0 / Cyclohexanols; 0 / Indoles; 0 / JHW 015; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Phenols; 0 / Protein Kinase Inhibitors; 0 / Receptors, Cannabinoid; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (25-35); 83003-12-7 / 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol; BBX060AN9V / Hydrogen Peroxide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  •  go-up   go-down


6. Hinkle CL, Diestel S, Lieberman J, Maness PF: Metalloprotease-induced ectodomain shedding of neural cell adhesion molecule (NCAM). J Neurobiol; 2006 Oct;66(12):1378-95
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.
  • [MeSH-minor] Amyloid Precursor Protein Secretases / metabolism. Animals. Antigens, CD / metabolism. Cell Line, Tumor. Cerebral Cortex / cytology. Cerebral Cortex / embryology. Cerebral Cortex / metabolism. Disease Models, Animal. Down-Regulation / physiology. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Fibroblasts / cytology. Fibroblasts / metabolism. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neurites / metabolism. Neurites / ultrastructure. Protein Structure, Tertiary / physiology. Protein Tyrosine Phosphatases / antagonists & inhibitors. Protein Tyrosine Phosphatases / metabolism. Schizophrenia / genetics. Schizophrenia / metabolism. Schizophrenia / physiopathology

  • COS Scholar Universe. author profiles.
  • 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
  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16967505.001).
  • [ISSN] 0022-3034
  • [Journal-full-title] Journal of neurobiology
  • [ISO-abbreviation] J. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH064065; United States / NINDS NIH HHS / NS / NS26620
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Neural Cell Adhesion Molecules; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / Adam8 protein, mouse; EC 3.4.24.81 / Adam10 protein, mouse
  •  go-up   go-down


7. Yang X, Sheng W, He Y, Cui J, Haidekker MA, Sun GY, Lee JC: Secretory phospholipase A2 type III enhances alpha-secretase-dependent amyloid precursor protein processing through alterations in membrane fluidity. J Lipid Res; 2010 May;51(5):957-66
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] Secretory phospholipase A2 type III enhances alpha-secretase-dependent amyloid precursor protein processing through alterations in membrane fluidity.
  • In the non-amyloidogenic pathway, amyloid precursor protein (APP) is cleaved by alpha-secretases to produce alpha-secretase-cleaved soluble APP (sAPP(alpha)) with neuroprotective and neurotrophic properties; therefore, enhancing the non-amyloidogenic pathway has been suggested as a potential pharmacological approach for the treatment of Alzheimer's disease.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PALMITIC ACID .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurobiol Aging. 2007 Aug;28(8):1179-86 [16790296.001]
  • [Cites] Brain Res. 2003 Oct 24;988(1-2):20-8 [14519523.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11735-40 [14504402.001]
  • [Cites] J Neurosci Res. 2003 Nov 1;74(3):342-52 [14598310.001]
  • [Cites] J Lipid Res. 2004 Feb;45(2):205-13 [14657205.001]
  • [Cites] J Biol Chem. 2004 Mar 19;279(12):11984-91 [14715666.001]
  • [Cites] J Mol Neurosci. 2004;23(1-2):105-14 [15126696.001]
  • [Cites] J Biol Chem. 2004 Oct 22;279(43):44945-54 [15322084.001]
  • [Cites] Jpn J Exp Med. 1982 Aug;52(4):183-92 [6129336.001]
  • [Cites] Neurosci Lett. 1987 Aug 18;79(1-2):195-200 [3670729.001]
  • [Cites] Acta Neuropathol. 1989;78(3):310-6 [2763803.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10307-11 [1946449.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Nov 27;181(1):265-71 [1958195.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):3055-9 [1557413.001]
  • [Cites] Nat Clin Pract Neurol. 2007 Jul;3(7):374-82 [17611486.001]
  • [Cites] J Cell Mol Med. 2007 May-Jun;11(3):383-92 [17635634.001]
  • [Cites] Biochem J. 2008 Jan 15;409(2):429-38 [17868035.001]
  • [Cites] J Neurochem. 2008 Feb;104(4):1116-31 [17995931.001]
  • [Cites] Neurobiol Aging. 2008 Apr;29(4):554-65 [17187903.001]
  • [Cites] Biochim Biophys Acta. 2008 Apr;1778(4):1148-53 [18258179.001]
  • [Cites] Neuron. 2008 Apr 10;58(1):42-51 [18400162.001]
  • [Cites] Science. 2008 Apr 25;320(5875):520-3 [18436784.001]
  • [Cites] Biochem Biophys Res Commun. 2008 May 30;370(2):207-12 [18374657.001]
  • [Cites] J Biol Chem. 2008 May 23;283(21):14257-68 [18353773.001]
  • [Cites] Nat Neurosci. 2008 Nov;11(11):1311-8 [18931664.001]
  • [Cites] J Neurosci. 2008 Nov 12;28(46):12052-61 [19005070.001]
  • [Cites] Biochim Biophys Acta. 2009 May;1788(5):964-72 [19366591.001]
  • [Cites] J Neurosci. 1995 Mar;15(3 Pt 2):2157-67 [7891158.001]
  • [Cites] J Biol Chem. 1996 Dec 20;271(51):32722-8 [8955105.001]
  • [Cites] J Biol Chem. 1997 Mar 14;272(11):7173-81 [9054413.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Jul 9;236(1):59-65 [9223426.001]
  • [Cites] Neurobiol Dis. 1996 Feb;3(1):51-63 [9173912.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7492-6 [10713052.001]
  • [Cites] JAMA. 2000 Mar 22-29;283(12):1615-7 [10735401.001]
  • [Cites] Arch Neurol. 2000 Oct;57(10):1439-43 [11030795.001]
  • [Cites] Chem Biol. 2001 Feb;8(2):123-31 [11251287.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5815-20 [11309494.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5856-61 [11296263.001]
  • [Cites] J Neurosci Res. 2002 Mar 1;67(5):634-45 [11891776.001]
  • [Cites] J Neurosci Res. 2002 Jun 1;68(5):558-67 [12111845.001]
  • [Cites] Ann Neurol. 2002 Sep;52(3):346-50 [12205648.001]
  • [Cites] J Mol Neurosci. 2002 Aug-Oct;19(1-2):31-5 [12212790.001]
  • [Cites] J Neurosci Res. 2002 Nov 1;70(3):462-73 [12391607.001]
  • [Cites] Biochemistry. 2002 Nov 26;41(47):13982-8 [12437355.001]
  • [Cites] J Cell Biol. 2003 Jan 6;160(1):113-23 [12515826.001]
  • [Cites] J Biol Chem. 2003 Mar 21;278(12):10657-67 [12522102.001]
  • [Cites] J Cell Sci. 2003 Aug 15;116(Pt 16):3339-46 [12829747.001]
  • [Cites] J Biol Chem. 2003 Aug 15;278(33):31261-8 [12761223.001]
  • [Cites] J Mol Neurosci. 2003;20(3):233-9 [14501002.001]
  • [Cites] Neuron. 1992 Jul;9(1):129-37 [1632967.001]
  • [Cites] J Biol Chem. 1993 Feb 15;268(5):3021-4 [8428976.001]
  • [Cites] Neuron. 1993 Feb;10(2):243-54 [8094963.001]
  • [Cites] Cell. 1989 Aug 25;58(4):615-22 [2475254.001]
  • [Cites] Science. 1990 Jun 1;248(4959):1122-4 [2111583.001]
  • [Cites] Neurosci Lett. 1990 Oct 30;119(1):32-6 [2097581.001]
  • [Cites] Ann N Y Acad Sci. 1993 Sep 24;695:128-31 [8239270.001]
  • [Cites] J Biol Chem. 1994 Jul 1;269(26):17386-9 [8021238.001]
  • [Cites] Am J Pathol. 1998 Jan;152(1):307-17 [9422548.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6460-4 [9600988.001]
  • [Cites] Circ Res. 1998 Nov 2;83(9):923-31 [9797341.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1627-31 [10362785.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1673-84 [10362792.001]
  • [Cites] Glia. 1999 Aug;27(2):110-28 [10417811.001]
  • [Cites] J Neurochem. 1999 Aug;73(2):532-7 [10428048.001]
  • [Cites] Neuroreport. 2004 Dec 3;15(17):2677-80 [15570177.001]
  • [Cites] J Cell Biol. 2004 Dec 6;167(5):809-12 [15583026.001]
  • [Cites] J Cell Biol. 2004 Dec 6;167(5):953-60 [15583033.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):18696-702 [15778502.001]
  • [Cites] J Biol Chem. 2005 Jul 1;280(26):24987-98 [15863501.001]
  • [Cites] Free Radic Biol Med. 2006 Feb 1;40(3):376-87 [16443152.001]
  • [Cites] Neurosci Lett. 2006 Apr 24;397(3):214-8 [16406345.001]
  • [Cites] Neuroscientist. 2006 Jun;12(3):245-60 [16684969.001]
  • [Cites] Brain Res. 2006 Jun 13;1094(1):38-46 [16697978.001]
  • [Cites] Neuron. 2006 Oct 5;52(1):15-31 [17015224.001]
  • [Cites] J Neurosci. 2006 Oct 25;26(43):11111-9 [17065451.001]
  • (PMID = 19805624.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / P01 AG018357; United States / NINDS NIH HHS / NS / R21 NS052385; United States / NIA NIH HHS / AG / 1P01 AG18357; United States / NINDS NIH HHS / NS / 1R21 NS052385
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Lysophosphatidylcholines; 27YG812J1I / Arachidonic Acid; 2V16EO95H1 / Palmitic Acid; EC 3.1.1.4 / Group III Phospholipases A2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / Bace protein, rat
  • [Other-IDs] NLM/ PMC2853463
  •  go-up   go-down


8. Chen CH, Wang PH, Liu BH, Hsu HH, Mersmann HJ, Ding ST: Serum amyloid A protein regulates the expression of porcine genes related to lipid metabolism. J Nutr; 2008 Apr;138(4):674-9
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.
  • [Title] Serum amyloid A protein regulates the expression of porcine genes related to lipid metabolism.
  • Serum amyloid A protein (SAA) is an apolipoprotein that can replace apolipoprotein A1 (apoA1) as the major apolipoprotein of HDL.
  • SAA treatment also increased inflammatory cytokine gene expression (IL-6 and tumor necrosis factor alpha) and glycerol release (P < 0.05), indicating increased lipolysis.
  • [MeSH-major] Gene Expression Regulation / drug effects. Lipid Metabolism / drug effects. Lipid Metabolism / genetics. Serum Amyloid A Protein / pharmacology. Swine / genetics. Swine / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18356319.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Serum Amyloid A Protein; 25167-62-8 / Docosahexaenoic Acids
  •  go-up   go-down


9. Sun X, Wu WH, Liu Q, Chen MS, Yu YP, Ma Y, Zhao YF, Li YM: Hybrid peptides attenuate cytotoxicity of beta-amyloid by inhibiting its oligomerization: implication from solvent effects. Peptides; 2009 Jul;30(7):1282-7
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] Hybrid peptides attenuate cytotoxicity of beta-amyloid by inhibiting its oligomerization: implication from solvent effects.
  • Abnormal assembly of monomeric beta-amyloid (Abeta) in Alzheimer's disease leads to the formation of most neurotoxic oligomers in vivo.
  • [MeSH-major] Amyloid beta-Peptides / chemistry. Amyloid beta-Peptides / toxicity. Neurons / drug effects. Peptides / chemistry. Peptides / pharmacology. Protein Multimerization / drug effects
  • [MeSH-minor] Amino Acid Motifs. Amino Acid Sequence. Animals. Cell Line, Tumor. Mice. Microscopy, Electron, Transmission. Molecular Sequence Data

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19397942.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Peptides
  •  go-up   go-down


11. Bräuner EV, Forchhammer L, Møller P, Barregard L, Gunnarsen L, Afshari A, Wåhlin P, Glasius M, Dragsted LO, Basu S, Raaschou-Nielsen O, Loft S: Indoor particles affect vascular function in the aged: an air filtration-based intervention study. Am J Respir Crit Care Med; 2008 Feb 15;177(4):419-25
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.
  • Secondary endpoints included hemoglobin, red blood cells, platelet count, coagulation factors, P-selectin, plasma amyloid A, C-reactive protein, fibrinogen, IL-6, tumor necrosis factor-alpha, protein oxidation measured as 2-aminoadipic semialdehyde in plasma, urinary 8-iso-prostaglandin F(2alpha), and blood pressure.


12. Wang CY, Wang T, Zheng W, Zhao BL, Danscher G, Chen YH, Wang ZY: Zinc overload enhances APP cleavage and Aβ deposition in the Alzheimer mouse brain. PLoS One; 2010;5(12):e15349
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: Abnormal zinc homeostasis is involved in β-amyloid (Aβ) plaque formation and, therefore, the zinc load is a contributing factor in Alzheimer's disease (AD).
  • However, the involvement of zinc in amyloid precursor protein (APP) processing and Aβ deposition has not been well established in AD animal models in vivo.
  • [MeSH-major] Amyloid beta-Protein Precursor / metabolism. Zinc / metabolism
  • [MeSH-minor] Alzheimer Disease / metabolism. Animals. Cell Line, Tumor. Homeostasis. Humans. Learning. Male. Maze Learning. Memory. Mice. Mice, Transgenic. Models, Biological. Presenilin-1 / genetics. Risk Factors

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brain Res. 1998 Jul 13;799(1):97-107 [9666092.001]
  • [Cites] J Neurol Sci. 1998 Jun 11;158(1):47-52 [9667777.001]
  • [Cites] Met Ions Biol Syst. 1999;36:309-64 [10093929.001]
  • [Cites] Brain Res. 1999 Mar 27;823(1-2):88-95 [10095015.001]
  • [Cites] Exp Neurol. 1999 Aug;158(2):328-37 [10415140.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23223-8 [10438495.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 13;100(10):6157-62 [12724524.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11065-9 [12920183.001]
  • [Cites] Arch Neurol. 2003 Dec;60(12):1685-91 [14676042.001]
  • [Cites] Am J Pathol. 1999 Sep;155(3):853-62 [10487842.001]
  • [Cites] Int J Exp Pathol. 2005 Jun;86(3):147-59 [15910549.001]
  • [Cites] Histochem Cell Biol. 2005 Jun;123(6):605-11 [15981003.001]
  • [Cites] Mitochondrion. 2005 Feb;5(1):55-65 [16060292.001]
  • [Cites] Neurotox Res. 2005;7(4):265-71 [16179263.001]
  • [Cites] Neurotox Res. 2005;7(4):273-81 [16179264.001]
  • [Cites] Exp Dermatol. 2005 Nov;14(11):844-53 [16232307.001]
  • [Cites] Cochrane Database Syst Rev. 2006;(1):CD005380 [16437529.001]
  • [Cites] FASEB J. 2006 Jun;20(8):1212-4 [16627626.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 May;65(5):489-98 [16772872.001]
  • [Cites] J Struct Biol. 2006 Jul;155(1):30-7 [16325427.001]
  • [Cites] Br J Dermatol. 2006 Jul;155(1):39-49 [16792750.001]
  • [Cites] Prog Histochem Cytochem. 2006;41(2):57-139 [16949439.001]
  • [Cites] Neuroscience. 2006 Nov 17;143(1):63-72 [16962711.001]
  • [Cites] Biochemistry. 2007 Sep 18;46(37):10655-63 [17718543.001]
  • [Cites] Neuroscience. 2007 Dec 5;150(2):357-69 [17949919.001]
  • [Cites] Recent Pat CNS Drug Discov. 2007 Nov;2(3):180-7 [18221229.001]
  • [Cites] J Neurochem. 2008 Mar;104(5):1249-59 [18289347.001]
  • [Cites] Curr Opin Chem Biol. 2008 Apr;12(2):222-8 [18342639.001]
  • [Cites] Brain Res Bull. 2008 Sep 5;77(1):55-60 [18639746.001]
  • [Cites] J Exp Med. 2008 Nov 24;205(12):2781-9 [18955571.001]
  • [Cites] Biochim Biophys Acta. 2009 Jun;1793(6):1058-67 [19111579.001]
  • [Cites] Cell Mol Neurobiol. 2009 Jul;29(5):757-67 [19381799.001]
  • [Cites] Nat Rev Neurosci. 2009 Nov;10(11):780-91 [19826435.001]
  • [Cites] Neurobiol Aging. 2010 Jan;31(1):74-87 [18378045.001]
  • [Cites] FASEB J. 2009 Dec;23(12):4207-17 [19679638.001]
  • [Cites] J Neurosci. 2010 Feb 3;30(5):1631-6 [20130173.001]
  • [Cites] J Alzheimers Dis. 2010;20(1):323-31 [20164588.001]
  • [Cites] Ann Neurol. 1999 Dec;46(6):860-6 [10589538.001]
  • [Cites] Brain Res. 2000 Jan 10;852(2):274-8 [10678753.001]
  • [Cites] Curr Opin Chem Biol. 2000 Apr;4(2):184-91 [10742195.001]
  • [Cites] J Neurosci. 1999 Jun 1;19(11):RC10 [10341271.001]
  • [Cites] Cell Mol Biol (Noisy-le-grand). 2000 Jun;46(4):785-95 [10875440.001]
  • [Cites] J Biol Chem. 2000 Jun 30;275(26):19439-42 [10801774.001]
  • [Cites] Neuron. 2001 Jun;30(3):665-76 [11430801.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Jul 27;285(4):959-64 [11467845.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):32293-9 [11423547.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7705-10 [12032347.001]
  • [Cites] Neurobiol Aging. 2002 Nov-Dec;23(6):1031-8 [12470799.001]
  • [Cites] Brain Res Brain Res Rev. 2003 Jan;41(1):44-56 [12505647.001]
  • [Cites] Biochemistry. 2003 Mar 18;42(10):2768-73 [12627941.001]
  • [Cites] J Neurochem. 2003 May;85(3):563-70 [12694382.001]
  • [Cites] J Neurosci. 2004 Mar 31;24(13):3453-9 [15056725.001]
  • [Cites] Neurobiol Aging. 2004 Nov-Dec;25(10):1315-21 [15465629.001]
  • [Cites] J Biol Chem. 1993 Aug 5;268(22):16109-12 [8344894.001]
  • [Cites] J Biol Chem. 1994 Apr 22;269(16):12152-8 [8163520.001]
  • [Cites] Science. 1994 Sep 2;265(5177):1464-7 [8073293.001]
  • [Cites] Neuroreport. 1996 May 17;7(7):1301-4 [8817554.001]
  • [Cites] Mol Chem Neuropathol. 1997 May;31(1):13-28 [9271002.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1716-21 [9990090.001]
  • (PMID = 21179415.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Presenilin-1; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ PMC3003690
  •  go-up   go-down


13. Gutwein P, Schramme A, Sinke N, Abdel-Bakky MS, Voss B, Obermüller N, Doberstein K, Koziolek M, Fritzsche F, Johannsen M, Jung K, Schaider H, Altevogt P, Ludwig A, Pfeilschifter J, Kristiansen G: Tumoural CXCL16 expression is a novel prognostic marker of longer survival times in renal cell cancer patients. Eur J Cancer; 2009 Feb;45(3):478-89
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.
  • Our immunohistochemical analysis on tissue microarray of renal cancer samples of 104 patients revealed that ADAM10 correlated significantly with tumour stage, pathological nodal status, M status and lymphangiosis carcinomatosa.
  • Importantly, high levels of CXCL16 expression in renal cancer tissue correlated with better survival of patients, and CXCL16 correlated inversely to the tumour stage.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Carcinoma, Renal Cell / metabolism. Chemokines, CXC / metabolism. Kidney Neoplasms / metabolism. Membrane Proteins / metabolism. Neoplasm Proteins / metabolism. Receptors, Chemokine / metabolism. Receptors, Scavenger / metabolism. Receptors, Virus / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Male

  • Genetic Alliance. consumer health - Kidney cancer.
  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19070478.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCL16 protein, human; 0 / CXCR6 protein, human; 0 / Chemokines, CXC; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Chemokine; 0 / Receptors, Scavenger; 0 / Receptors, Virus; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
  •  go-up   go-down


14. Greco SJ, Sarkar S, Johnston JM, Zhu X, Su B, Casadesus G, Ashford JW, Smith MA, Tezapsidis N: Leptin reduces Alzheimer's disease-related tau phosphorylation in neuronal cells. Biochem Biophys Res Commun; 2008 Nov 21;376(3):536-41
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.
  • Recently, it was shown that leptin can reduce amyloid beta levels both in vitro and in vivo.
  • Thus, leptin, which ameliorates both amyloid beta and tau-related pathological pathways, holds promise as a novel therapeutic for Alzheimer's disease.
  • [MeSH-minor] AMP-Activated Protein Kinases. Aminoimidazole Carboxamide / analogs & derivatives. Aminoimidazole Carboxamide / pharmacology. Cell Line, Tumor. Humans. Insulin / pharmacology. Multienzyme Complexes / antagonists & inhibitors. Multienzyme Complexes / metabolism. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Pyrazoles / pharmacology. Pyrimidines / pharmacology. Ribonucleotides / pharmacology. Signal Transduction

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 8;351(1):171-5 [17054914.001]
  • [Cites] Cell. 2006 Sep 8;126(5):955-68 [16959574.001]
  • [Cites] Eur J Neurosci. 2007 Dec;26(12):3429-36 [18052981.001]
  • [Cites] J Biol Chem. 2008 Jan 4;283(1):100-9 [17971449.001]
  • [Cites] J Neurosci Res. 2008 Jul;86(9):2091-9 [18335524.001]
  • [Cites] Neurobiol Aging. 2009 Sep;30(9):1483-9 [18358569.001]
  • [Cites] J Neurochem. 2008 Sep;106(5):1977-90 [18466320.001]
  • [Cites] Nature. 2000 Apr 6;404(6778):661-71 [10766253.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24977-83 [10818091.001]
  • [Cites] Dement Geriatr Cogn Disord. 2001 Mar-Apr;12(2):167-70 [11173891.001]
  • [Cites] Nature. 2002 Jan 17;415(6869):339-43 [11797013.001]
  • [Cites] Ann N Y Acad Sci. 2002 Jun;967:379-88 [12079865.001]
  • [Cites] Trends Pharmacol Sci. 2002 Jun;23(6):288-93 [12084635.001]
  • [Cites] Neuron. 2003 Jul 31;39(3):409-21 [12895417.001]
  • [Cites] Nature. 2004 Apr 1;428(6982):569-74 [15058305.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jul 2;319(3):993-1000 [15184080.001]
  • [Cites] Dev Biol. 1984 Jun;103(2):285-93 [6144603.001]
  • [Cites] J Biol Chem. 1997 Aug 1;272(31):19547-53 [9235959.001]
  • [Cites] J Neurochem. 1999 Feb;72(2):576-84 [9930729.001]
  • [Cites] Nature. 1999 Sep 2;401(6748):73-6 [10485707.001]
  • [Cites] FASEB J. 2004 Dec;18(15):1870-8 [15576490.001]
  • [Cites] J Neurosci. 2007 Dec 12;27(50):13635-48 [18077675.001]
  • (PMID = 18801339.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R43 AG029670; United States / NIA NIH HHS / AG / R43 AG029670-01A1; United States / NIA NIH HHS / AG / 1R43AG029670
  • [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 / (6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine; 0 / Insulin; 0 / Leptin; 0 / Multienzyme Complexes; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Ribonucleotides; 0 / tau Proteins; 360-97-4 / Aminoimidazole Carboxamide; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; F0X88YW0YK / AICA ribonucleotide
  • [Other-IDs] NLM/ NIHMS74881; NLM/ PMC2577167
  •  go-up   go-down


15. Buchhave P, Zetterberg H, Blennow K, Minthon L, Janciauskiene S, Hansson O: Soluble TNF receptors are associated with Aβ metabolism and conversion to dementia in subjects with mild cognitive impairment. Neurobiol Aging; 2010 Nov;31(11):1877-84
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.
  • OBJECTIVE: There is evidence supporting that tumor necrosis factor receptor (TNFR)-signaling can induce production of beta-amyloid (Aβ) in the brain.
  • Moreover, amyloid-induced toxicity has been shown to be dependent on TNFR-signaling.
  • CONCLUSION: TNFR-signaling might be involved in the early pathogenesis of AD and VaD, and could be associated with beta-amyloid metabolism.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid beta-Peptides / metabolism. Cognition Disorders / metabolism. Dementia, Vascular / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2008 Elsevier Inc. All rights reserved.
  • (PMID = 19070941.001).
  • [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 / Amyloid beta-Peptides; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II
  •  go-up   go-down


16. Shiels SA, Hasan SI, Darowski A: Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis. Age Ageing; 2005 Nov;34(6):648-9
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] Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis.
  • Further investigations showed that the mass contained amyloid protein.
  • With no evidence of systemic amyloidosis or malignancy a diagnosis of amyloidoma/amyloid tumour was made.
  • This is the largest amyloid tumour reported in the literature to date.
  • Clearly amyloidomas are rare, but patients can present acutely and may have a poor prognosis, especially when the tumour is of considerable size.
  • [MeSH-major] Amyloid Neuropathies / complications. Leg. Lumbosacral Plexus. Pain / etiology. Pelvis

  • MedlinePlus Health Information. consumer health - Pain.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16267196.001).
  • [ISSN] 0002-0729
  • [Journal-full-title] Age and ageing
  • [ISO-abbreviation] Age Ageing
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 10
  •  go-up   go-down


17. Lo BK, Yu M, Zloty D, Cowan B, Shapiro J, McElwee KJ: CXCR3/ligands are significantly involved in the tumorigenesis of basal cell carcinomas. Am J Pathol; 2010 May;176(5):2435-46
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] CXCR3/ligands are significantly involved in the tumorigenesis of basal cell carcinomas.
  • Basal cell carcinoma (BCC) is the most common skin malignancy encountered worldwide.
  • We hypothesized that CXC chemokines, small cytokines involved in inducing directed leukocyte chemotaxis, could play a key role in the modulation of BCC growth.
  • In this study, quantitative RT-PCR revealed that the chemokines CXCL9, 10, 11, and their receptor CXCR3 were significantly upregulated by an average 22.6-fold, 9.2-fold, 26.6-fold, and 4.9-fold, respectively in BCC tissue samples as compared with nonlesional skin epithelium.
  • Immunohistochemistry analysis revealed that CXCR3, CXCL10, and CXCL11, but not CXCL9, colocalized with cytokeratin 17 (K17) in BCC keratinocytes.
  • In addition, CXCR3 and its ligands were expressed in cells of the surrounding BCC stroma.
  • The chemokines and K17 were also expressed in cultured human immortalized HaCaT keratinocytes.
  • Exposure of HaCaT cells or primary BCC-derived cells to CXCL11 peptides in vitro significantly increased cell proliferation.
  • In primary BCC-derived cell cultures, addition of CXCL11 progressively selected for K17+/CXCR3+ co-expressing cells over time.
  • The expression of CXCR3 and its ligands in human BCC keratinocytes, the enhancement of keratinocyte cell proliferation by CXCL11, and the homogeneity of K17+ BCC cells in human BCC-isolated cell population supported by CXCR3/CXCL11 signaling all suggest that CXCR3 and its ligands may be important autocrine and/or paracrine signaling mediators in the tumorigenesis of BCC.

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 1999 May 31;145(5):927-32 [10352011.001]
  • [Cites] J Cell Biol. 1999 Oct 4;147(1):71-6 [10508856.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):596-9 [16522748.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):32-42 [17591951.001]
  • [Cites] Hum Pathol. 2007 Nov;38(11):1676-87 [17707463.001]
  • [Cites] Int J Cancer. 2008 Jan 1;122(1):50-6 [17721996.001]
  • [Cites] J Am Acad Dermatol. 2008 Jan;58(1):158-67 [18158927.001]
  • [Cites] N Engl J Med. 2008 Jan 24;358(4):393-401 [18216361.001]
  • [Cites] J Immunol Methods. 2008 Feb 29;331(1-2):140-6 [18234207.001]
  • [Cites] Am J Dermatopathol. 2008 Jun;30(3):249-55 [18496426.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2008 Jun;294(6):L1187-96 [18375741.001]
  • [Cites] J Invest Dermatol. 2008 Jul;128(7):1797-805 [18200053.001]
  • [Cites] J Neuroimmunol. 2008 Aug 13;199(1-2):35-45 [18538864.001]
  • [Cites] Am J Pathol. 2008 Sep;173(3):835-43 [18688030.001]
  • [Cites] Arch Dermatol Res. 2010 Mar;302(2):113-23 [19517126.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1285-91 [10545995.001]
  • [Cites] Int J Cancer. 1999 Dec 10;83(6):780-9 [10597195.001]
  • [Cites] J Immunol. 2000 Jan 15;164(2):733-8 [10623817.001]
  • [Cites] Br J Dermatol. 2000 Dec;143(6):1224-9 [11122025.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9945-54 [11136732.001]
  • [Cites] J Intern Med. 2001 Aug;250(2):91-104 [11489059.001]
  • [Cites] Am J Pathol. 2001 Oct;159(4):1567-79 [11583982.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45098-105 [11571298.001]
  • [Cites] Am J Dermatopathol. 2001 Dec;23(6):501-9 [11801790.001]
  • [Cites] Br J Dermatol. 2002 Apr;146 Suppl 61:1-6 [11966724.001]
  • [Cites] J Clin Invest. 2002 Oct;110(7):933-41 [12370271.001]
  • [Cites] Int J Dermatol. 2002 Oct;41(10):652-8 [12390187.001]
  • [Cites] J Histochem Cytochem. 2002 Nov;50(11):1425-34 [12417607.001]
  • [Cites] Leukemia. 2003 Jan;17(1):203-10 [12529679.001]
  • [Cites] J Invest Dermatol. 2003 Jul;121(1):191-7 [12839581.001]
  • [Cites] BMJ. 2003 Oct 4;327(7418):794-8 [14525881.001]
  • [Cites] Am J Pathol. 2003 Dec;163(6):2451-8 [14633617.001]
  • [Cites] Cancer Lett. 2004 Apr 30;207(2):221-7 [15072832.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):4010-7 [15173015.001]
  • [Cites] Cancer Metastasis Rev. 2004 Aug-Dec;23(3-4):389-402 [15197337.001]
  • [Cites] J Cell Biol. 1982 Oct;95(1):285-95 [6183270.001]
  • [Cites] J Invest Dermatol. 1983 Jul;81(1 Suppl):33s-40s [6345690.001]
  • [Cites] Lancet. 1987 Aug 22;2(8556):443-6 [2887739.001]
  • [Cites] J Cell Biol. 1988 Mar;106(3):761-71 [2450098.001]
  • [Cites] Br J Dermatol. 1990 Mar;122(3):399-403 [2322501.001]
  • [Cites] Int J Cancer. 1990 Sep 15;46(3):356-61 [2394501.001]
  • [Cites] J Am Acad Dermatol. 1990 Sep;23(3 Pt 1):413-21 [2212139.001]
  • [Cites] Dermatol Clin. 1991 Oct;9(4):751-5 [1934649.001]
  • [Cites] J Invest Dermatol. 1992 Jan;98(1):45-9 [1370231.001]
  • [Cites] Int J Cancer. 1993 Feb 20;53(4):585-90 [8436431.001]
  • [Cites] Carcinogenesis. 1993 May;14(5):833-9 [8504475.001]
  • [Cites] Acta Derm Venereol. 1993 Aug;73(4):286-92 [7506469.001]
  • [Cites] Oncogene. 1995 Sep 7;11(5):961-9 [7675455.001]
  • [Cites] Br J Dermatol. 1995 Oct;133(4):501-11 [7577575.001]
  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):78-81 [8782823.001]
  • [Cites] Am J Dermatopathol. 1997 Aug;19(4):341-50 [9261468.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):90-2 [9422511.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1050-5 [9448283.001]
  • [Cites] N Engl J Med. 1998 Feb 12;338(7):436-45 [9459648.001]
  • [Cites] J Photochem Photobiol B. 1998 Mar;42(3):167-79 [9595706.001]
  • [Cites] J Invest Dermatol. 1998 Jun;110(6):885-8 [9620294.001]
  • [Cites] Blood. 2000 Jan 15;95(2):627-32 [10627472.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3438-43 [10725363.001]
  • [Cites] J Immunol. 2004 Nov 15;173(10):6234-40 [15528361.001]
  • [Cites] Genes Dev. 2005 Jan 15;19(2):214-23 [15625189.001]
  • [Cites] J Dtsch Dermatol Ges. 2005 Jul;3(7):493-503 [15967008.001]
  • [Cites] Amyloid. 2005 Mar;12(1):41-7 [16076610.001]
  • [Cites] JAMA. 2005 Aug 10;294(6):681-90 [16091570.001]
  • [Cites] Carcinogenesis. 2005 Oct;26(10):1657-67 [15905207.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2006 May;290(5):L909-18 [16339779.001]
  • [Cites] Br J Dermatol. 2006 May;154(5):910-8 [16634895.001]
  • [Cites] Clin Cancer Res. 2006 Apr 15;12(8):2427-33 [16638848.001]
  • [Cites] Am J Dermatopathol. 2006 Aug;28(4):293-307 [16871032.001]
  • [Cites] Exp Dermatol. 2006 Sep;15(9):667-77 [16881963.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9509-18 [17018607.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14842-7 [17003113.001]
  • [Cites] Haematologica. 2006 Nov;91(11):1489-97 [17082008.001]
  • [Cites] Eur J Immunol. 2007 Feb;37(2):338-50 [17274000.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3396-405 [17409450.001]
  • [Cites] Endocrinology. 2007 May;148(5):2317-25 [17255201.001]
  • [Cites] Int J Exp Pathol. 2000 Jun;81(3):183-9 [10971739.001]
  • [Cites] J Dermatol Sci. 1998 May;17(1):15-23 [9651824.001]
  • [Cites] Int J Cancer. 1998 Nov 23;78(5):587-93 [9808527.001]
  • [Cites] Eur J Immunol. 1998 Nov;28(11):3696-705 [9842912.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 2):2682-6 [10068274.001]
  • [CommentIn] Am J Pathol. 2010 May;176(5):2088-91 [20185576.001]
  • (PMID = 20228225.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MUS-94025
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL11 protein, human; 0 / Chemokine CXCL11; 0 / Ligands; 0 / Receptors, CXCR3
  • [Other-IDs] NLM/ PMC2861108
  •  go-up   go-down


18. Kauf AC, Rosenbusch RF, Paape MJ, Bannerman DD: Innate immune response to intramammary Mycoplasma bovis infection. J Dairy Sci; 2007 Jul;90(7):3336-48
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.
  • Acute phase protein synthesis, which reflects 1 parameter of the systemic response to infection, was induced within 108 h of infection, as evidenced by increased circulating concentrations of lipopolysaccharide binding protein and serum amyloid A.
  • Milk concentrations of several cytokines, including IFN-gamma, IL-1beta, IL-10, IL-12, tumor growth factor-alpha, and tumor necrosis factor-alpha, were elevated in response to infection over a period of several days, whereas increases in milk IL-8 were of a more limited duration.

  • Hazardous Substances Data Bank. AFLATOXIN B1 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17582119.001).
  • [ISSN] 1525-3198
  • [Journal-full-title] Journal of dairy science
  • [ISO-abbreviation] J. Dairy Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Serum Albumin; 0 / aflatoxin B1-bovine serum albumin; 80295-54-1 / Complement C5a; 9N2N2Y55MH / Aflatoxin B1
  •  go-up   go-down


19. Kerr ML, Gasperini R, Gibbs ME, Hou X, Shepherd CE, Strickland DK, Foa L, Lawen A, Small DH: Inhibition of Abeta aggregation and neurotoxicity by the 39-kDa receptor-associated protein. J Neurochem; 2010 Mar;112(5):1199-209
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.
  • Aggregation of beta-amyloid protein (Abeta) to form oligomers is considered to be a key step in generating neurotoxicity in the Alzheimer's disease brain.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. LDL-Receptor Related Protein-Associated Protein / therapeutic use. Neurotoxicity Syndromes / drug therapy. Neurotoxicity Syndromes / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Animals, Newborn. Avoidance Learning / drug effects. Behavior, Animal. Cell Line, Tumor. Chickens. Discrimination Learning / drug effects. Disease Models, Animal. Flow Cytometry / methods. Fluorescein / metabolism. Humans. Immunoprecipitation / methods. Memory / drug effects. Microscopy, Atomic Force / methods. Microscopy, Confocal / methods. Molecular Weight. Neuroblastoma. Nuclear Proteins / metabolism. Peptide Fragments / metabolism. Peptide Fragments / pharmacology. Protein Binding. Protein Transport / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUORESCEIN .
  • Hazardous Substances Data Bank. D&C Yellow No. 8 .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20002523.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL50784; United States / NHLBI NIH HHS / HL / HL54710
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / LDL-Receptor Related Protein-Associated Protein; 0 / Nuclear Proteins; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); TPY09G7XIR / Fluorescein
  •  go-up   go-down


20. Cantarella G, Di Benedetto G, Pezzino S, Risuglia N, Bernardini R: TRAIL-related neurotoxicity implies interaction with the Wnt pathway in human neuronal cells in vitro. J Neurochem; 2008 Jun;105(5):1915-23
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.
  • Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is involved in amyloid beta dependent neurotoxicity via the extrinsic pathway.
  • Recently, several genes modulating TRAIL cytotoxicity have been characterized, providing evidence for a role of wingless-type mouse mammary tumor virus integration site family (Wnt), Jun-N-terminal kinase and other pathways in increased cell susceptibility to the cytokine.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cell Line, Tumor. Humans

  • 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 = 18266928.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Wnt Proteins
  •  go-up   go-down


21. Staropoli JF: Tumorigenesis and neurodegeneration: two sides of the same coin? Bioessays; 2008 Aug;30(8):719-27
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.
  • Increased dosage of amyloid precursor protein in Down syndrome (trisomy 21) predisposes to dementia of Alzheimer type and may also contribute to acute leukemia and transient myeloproliferative disorder.
  • The gene parkin, loss-of-function mutations in which account for about half of cases of early-onset Parkinson disease, has been identified as a candidate tumor suppressor gene by several groups.
  • Parkin is deleted or downregulated in several tumor types, and its re-expression sensitizes derivative cell lines to inhibitors of cell-cycle progression.
  • [MeSH-minor] Amyloid / metabolism. Animals. Ataxia Telangiectasia Mutated Proteins. Biomarkers / metabolism. Cell Cycle. Cell Cycle Proteins / metabolism. DNA-Binding Proteins / metabolism. Down Syndrome / genetics. Down Syndrome / pathology. Humans. Models, Biological. Mutation. Neurons / metabolism. Parkinson Disease / genetics. Parkinson Disease / pathology. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Degenerative Nerve Diseases.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley Periodicals, Inc.
  • (PMID = 18623069.001).
  • [ISSN] 1521-1878
  • [Journal-full-title] BioEssays : news and reviews in molecular, cellular and developmental biology
  • [ISO-abbreviation] Bioessays
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Biomarkers; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Number-of-references] 90
  •  go-up   go-down


22. Dong Y, Zhang G, Zhang B, Moir RD, Xia W, Marcantonio ER, Culley DJ, Crosby G, Tanzi RE, Xie Z: The common inhalational anesthetic sevoflurane induces apoptosis and increases beta-amyloid protein levels. Arch Neurol; 2009 May;66(5):620-31
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] The common inhalational anesthetic sevoflurane induces apoptosis and increases beta-amyloid protein levels.
  • OBJECTIVE: To assess the effects of sevoflurane, the most commonly used inhalation anesthetic, on apoptosis and beta-amyloid protein (Abeta) levels in vitro and in vivo.
  • Subjects Naive mice, H4 human neuroglioma cells, and H4 human neuroglioma cells stably transfected to express full-length amyloid precursor protein.
  • INTERVENTIONS: Human H4 neuroglioma cells stably transfected to express full-length amyloid precursor protein were exposed to 4.1% sevoflurane for 6 hours.
  • RESULTS: Sevoflurane induced apoptosis and elevated levels of beta-site amyloid precursor protein-cleaving enzyme and Abeta in vitro and in vivo.
  • These results suggest that sevoflurane induces caspase activation which, in turn, enhances beta-site amyloid precursor protein-cleaving enzyme and Abeta levels.

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Sevoflurane .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Stroke. 2004 Mar;35(3):758-63 [14963280.001]
  • [Cites] J Biol Chem. 2008 May 2;283(18):11866-75 [18326038.001]
  • [Cites] Eur J Anaesthesiol. 2004 Jul;21(7):530-7 [15318464.001]
  • [Cites] Anesthesiology. 2004 Sep;101(3):710-21 [15329596.001]
  • [Cites] Biochem Biophys Res Commun. 1984 Aug 16;122(3):1131-5 [6236805.001]
  • [Cites] Stroke. 1990 Oct;21(10):1485-8 [2219214.001]
  • [Cites] Int J Neurosci. 1994 Aug;77(3-4):181-5 [7814211.001]
  • [Cites] Anesthesiology. 1995 Jan;82(1):305-7 [7832317.001]
  • [Cites] Neuroreport. 1994 Dec 20;5(18):2529-33 [7696596.001]
  • [Cites] Acta Neuropathol. 1996;91(1):61-6 [8773147.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Jan;56(1):86-93 [8990132.001]
  • [Cites] Science. 1997 Jul 18;277(5324):373-6 [9219695.001]
  • [Cites] J Biol Chem. 1997 Aug 15;272(33):20655-9 [9252383.001]
  • [Cites] Nat Med. 1997 Sep;3(9):954-5 [9288715.001]
  • [Cites] Stroke. 1998 Mar;29(3):695-704 [9506615.001]
  • [Cites] J Neurosci. 1998 May 15;18(10):3659-68 [9570797.001]
  • [Cites] Chem Biol. 1998 May;5(5):R97-103 [9578633.001]
  • [Cites] J Neurosci. 1998 Aug 1;18(15):5869-80 [9671674.001]
  • [Cites] Essays Biochem. 1998;33:149-63 [10488448.001]
  • [Cites] Anesthesiology. 2004 Dec;101(6):1313-24 [15564938.001]
  • [Cites] Brain Res. 2005 Feb 9;1034(1-2):147-52 [15713266.001]
  • [Cites] Cell. 2005 Feb 25;120(4):545-55 [15734686.001]
  • [Cites] Brain Res. 2005 Mar 10;1037(1-2):139-47 [15777762.001]
  • [Cites] J Mol Neurosci. 2005;25(1):67-77 [15781968.001]
  • [Cites] J Biol Chem. 2005 Apr 15;280(15):15413-21 [15699037.001]
  • [Cites] Anesthesiology. 2005 Jun;102(6):1147-57 [15915027.001]
  • [Cites] Stroke. 2005 Jul;36(7):1551-6 [15933257.001]
  • [Cites] Life Sci. 2005 Sep 23;77(19):2369-83 [15993426.001]
  • [Cites] J Alzheimers Dis. 2005 Aug;7(4):319-24 [16131734.001]
  • [Cites] J Neurochem. 1999 Dec;73(6):2278-85 [10582585.001]
  • [Cites] EMBO Rep. 2001 Sep;2(9):835-41 [11520861.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35235-8 [11483588.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):43756-60 [11583985.001]
  • [Cites] Anesthesiology. 2001 Dec;95(6):1467-72 [11748407.001]
  • [Cites] Int Rev Neurobiol. 2002;53:387-409 [12512347.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):715-20 [12522260.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2003 Apr;27(2):251-4 [12657364.001]
  • [Cites] J Appl Physiol (1985). 2005 Nov;99(5):2028-35 [16002771.001]
  • [Cites] J Neurosci. 2005 Nov 23;25(47):10874-83 [16306400.001]
  • [Cites] Anesthesiology. 2006 May;104(5):988-94 [16645451.001]
  • [Cites] Anesth Analg. 2006 Jul;103(1):173-9, table of contents [16790648.001]
  • [Cites] Food Chem Toxicol. 2006 Aug;44(8):1399-407 [16678324.001]
  • [Cites] Circulation. 2006 Jul 4;114(1 Suppl):I226-32 [16820577.001]
  • [Cites] Biomed Environ Sci. 2006 Apr;19(2):143-6 [16827187.001]
  • [Cites] Anesthesiology. 2006 Nov;105(5):990-8 [17065894.001]
  • [Cites] J Gerontol A Biol Sci Med Sci. 2006 Dec;61(12):1300-6 [17234824.001]
  • [Cites] J Neurosci. 2007 Feb 7;27(6):1247-54 [17287498.001]
  • [Cites] Neuron. 2007 Jun 7;54(5):721-37 [17553422.001]
  • [Cites] Am J Nephrol. 2007;27(4):416-24 [17622749.001]
  • [Cites] Neurosci Lett. 2007 Sep 20;425(1):59-62 [17723266.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1722-7 [18227504.001]
  • [Cites] Anesth Analg. 2008 Apr;106(4):1150-60, table of contents [18349187.001]
  • [Cites] J Neurosci. 2008 Apr 23;28(17):4551-60 [18434534.001]
  • [Cites] Anesthesiology. 2004 Apr;100(4):1038-9; author reply 1039-40 [15087655.001]
  • (PMID = 19433662.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS048140-05; United States / NIA NIH HHS / AG / R21 AG029856; United States / NIA NIH HHS / AG / AG029856; United States / NINDS NIH HHS / NS / NS048140-05; United States / NINDS NIH HHS / NS / K08 NS048140-04; United States / NIGMS NIH HHS / GM / R01 GM088801; United States / NIGMS NIH HHS / GM / GM077507; United States / NIA NIH HHS / AG / AG2025; United States / NIA NIH HHS / AG / AG029856-01A2; United States / NINDS NIH HHS / NS / NS048140-04; United States / NINDS NIH HHS / NS / NS048140; United States / NINDS NIH HHS / NS / K08 NS048140; United States / NIGMS NIH HHS / GM / GM088801-01A1; United States / NIGMS NIH HHS / GM / R01 GM088801-01A1; United States / NIA NIH HHS / AG / R21 AG029856-01A2; United States / NIGMS NIH HHS / GM / GM088801
  • [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 / Amyloid beta-Peptides; 0 / Anesthetics, Inhalation; 0 / Enzyme Inhibitors; 0 / Methyl Ethers; 38LVP0K73A / sevoflurane; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS130512; NLM/ PMC2748878
  •  go-up   go-down


23. Clementz AG, Osipo C: Notch versus the proteasome: what is the target of gamma-secretase inhibitor-I? Breast Cancer Res; 2009;11(5):110
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.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Receptors, Notch / antagonists & inhibitors
  • [MeSH-minor] Cell Line, Tumor. Female. Humans. Leupeptins / pharmacology. Oligopeptides / pharmacology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mammary Gland Biol Neoplasia. 2001 Jan;6(1):23-36 [11467450.001]
  • [Cites] Endocr Relat Cancer. 2004 Sep;11(3):497-522 [15369451.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8530-7 [16166334.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 18;99(8):616-27 [17440163.001]
  • [Cites] Ann Oncol. 2008 May;19(5):871-6 [18209010.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):5226-35 [18593923.001]
  • [Cites] Oncogene. 2008 Aug 28;27(37):5019-32 [18469855.001]
  • [Cites] Oncogene. 2008 Sep 1;27(38):5124-31 [18758481.001]
  • [Cites] Clin Cancer Res. 2009 Mar 15;15(6):2010-21 [19276287.001]
  • [Cites] Br J Cancer. 2009 Jun 16;100(12):1879-88 [19513078.001]
  • [Cites] Cancer Res. 2009 Jun 15;69(12):5015-22 [19491273.001]
  • [Cites] Breast Cancer Res. 2009;11(4):R57 [19660128.001]
  • [CommentOn] Breast Cancer Res. 2009;11(4):R57 [19660128.001]
  • (PMID = 19849815.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Leupeptins; 0 / Oligopeptides; 0 / Receptors, Notch; 0 / benzyloxycarbonyl-leucyl-leucyl-norleucinal; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2790851
  •  go-up   go-down


24. Behle JH, Sedaghatfar MH, Demmer RT, Wolf DL, Celenti R, Kebschull M, Belusko PB, Herrera-Abreu M, Lalla E, Papapanou PN: Heterogeneity of systemic inflammatory responses to periodontal therapy. J Clin Periodontol; 2009 Apr;36(4):287-94
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, only sE-selectin, sICAM, and serum amyloid P sustained a reduction at T4.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oral Microbiol Immunol. 1997 Oct;12(5):303-10 [9467384.001]
  • [Cites] Clin Exp Immunol. 1997 Feb;107(2):347-52 [9030874.001]
  • [Cites] N Engl J Med. 1999 Jan 14;340(2):115-26 [9887164.001]
  • [Cites] J Periodontal Res. 2005 Feb;40(1):53-8 [15613080.001]
  • [Cites] J Dent Res. 2005 Mar;84(3):269-73 [15723869.001]
  • [Cites] N Engl J Med. 2005 Apr 21;352(16):1685-95 [15843671.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2005 Jun;25(6):1102-11 [15790935.001]
  • [Cites] J Clin Periodontol. 2005 Oct;32(10):1055-61 [16174268.001]
  • [Cites] J Periodontol. 2005 Nov;76(11 Suppl):2089-100 [16277581.001]
  • [Cites] J Periodontol. 2005 Nov;76(11 Suppl):2106-15 [16277583.001]
  • [Cites] Am Heart J. 2006 Jan;151(1):47 [16368290.001]
  • [Cites] Lipids. 2005 Dec;40(12):1215-20 [16477805.001]
  • [Cites] J Thromb Haemost. 2006 Oct;4(10):2256-61 [16856978.001]
  • [Cites] Atherosclerosis. 2007 Feb;190(2):271-81 [16620832.001]
  • [Cites] J Clin Periodontol. 2007 Feb;34(2):124-9 [17214734.001]
  • [Cites] N Engl J Med. 2007 Mar 1;356(9):911-20 [17329698.001]
  • [Cites] J Periodontol. 2007 Apr;78(4):683-90 [17397316.001]
  • [Cites] J Periodontal Res. 2007 Jun;42(3):274-82 [17451548.001]
  • [Cites] J Clin Periodontol. 2007 Jul;34(7):574-80 [17535288.001]
  • [Cites] J Clin Periodontol. 2007 Sep;34(9):736-47 [17716309.001]
  • [Cites] J Lipid Res. 2007 Oct;48(10):2162-71 [17630380.001]
  • [Cites] J Clin Periodontol. 2008 Apr;35(4):277-90 [18294231.001]
  • [Cites] J Periodontol. 2000 Jun;71(6):885-97 [10914791.001]
  • [Cites] J Periodontol. 2000 Oct;71(10):1528-34 [11063384.001]
  • [Cites] J Periodontol. 2001 Sep;72(9):1221-7 [11577954.001]
  • [Cites] Lancet. 2001 Sep 22;358(9286):971-6 [11583751.001]
  • [Cites] Infect Immun. 2002 Jan;70(1):257-67 [11748191.001]
  • [Cites] Prog Cardiovasc Nurs. 2003 Winter;18(1):42-9 [12624571.001]
  • [Cites] J Dent Res. 2004 Feb;83(2):156-60 [14742655.001]
  • [Cites] J Periodontol. 2004 Mar;75(3):420-8 [15088881.001]
  • [Cites] J Clin Periodontol. 2004 Nov;31(11):985-90 [15491314.001]
  • [Cites] J Dent Res. 1967 May-Jun;46(3):624 [5229585.001]
  • [Cites] J Periodontol. 1968 Mar;39(2):93-5 [5239780.001]
  • [Cites] Annu Rev Immunol. 1993;11:767-804 [8476577.001]
  • [Cites] Periodontol 2000. 1994 Jun;5:78-111 [9673164.001]
  • (PMID = 19426174.001).
  • [ISSN] 1600-051X
  • [Journal-full-title] Journal of clinical periodontology
  • [ISO-abbreviation] J. Clin. Periodontol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / K99 DE-018739; United States / NIDCR NIH HHS / DE / DE015649-03; United States / NIDCR NIH HHS / DE / DE015649-02; United States / NIDCR NIH HHS / DE / R01 DE015649-03; United States / NIDCR NIH HHS / DE / DE015649; United States / NIDCR NIH HHS / DE / R01 DE015649; United States / NIDCR NIH HHS / DE / K99 DE018739; United States / NIDCR NIH HHS / DE / R01 DE015649-02
  • [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 / Adiponectin; 0 / Antibodies, Bacterial; 0 / E-Selectin; 0 / Inflammation Mediators; 0 / Interleukins; 0 / Plasminogen Activator Inhibitor 1; 0 / Serum Amyloid P-Component; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 9007-41-4 / C-Reactive Protein; EC 1.11.1.7 / Peroxidase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS133569; NLM/ PMC2753407
  •  go-up   go-down


25. Saruc M, Iki K, Pour PM: Morphometric studies in human pancreatic cancer argues against the etiological role of type 2 diabetes in pancreatic cancer. Histol Histopathol; 2010 04;25(4):423-32
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.
  • BACKGROUND: To understand the role of islet amyloid polypeptide (IAPP) in type 2 diabetes and pancreatic cancer (PC), we investigated the patterns of its expression and its ratio to insulin, glucagon, somatostatin and pancreatic polypeptide cells by morphometry in tissues from these two diseases in comparison to the normal pancreas.
  • MATERIALS AND METHODS: Pancreatic tissues from 11 donors (five without pancreatic disease and six with type 2 diabetes) and 11 surgical specimens from PC patients obtained from the cancer area (zone A) and the adjacent tumor-free area (zone B) were examined immunohistochemically.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amyloid / metabolism. Biomarkers, Tumor / metabolism. Female. Glucagon / metabolism. Humans. Immunoenzyme Techniques. Insulin / metabolism. Islet Amyloid Polypeptide. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Male. Middle Aged. Pancreatic Polypeptide / metabolism


26. Qi XL, Shan KR, Xiao Y, Liu RY, Gu R, Guan ZZ: [Influence of beta-amyloid peptide on cell membrane lipids and cholinergic receptors in human neuroblastoma SH-SY5Y cells]. Zhonghua Bing Li Xue Za Zhi; 2006 Jan;35(1):37-41
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] [Influence of beta-amyloid peptide on cell membrane lipids and cholinergic receptors in human neuroblastoma SH-SY5Y cells].
  • OBJECTIVE: To study the effects of beta-amyloid peptide (Abeta) on cell membrane lipids and cholinergic receptors of human neuroblastoma cells.
  • CONCLUSION: beta-amyloid peptide reduces the level of cell membrane lipids and cholinergic receptors in human SH-SY5Y neuroblastoma cells, likely through the induction of an enhanced oxidative stress.
  • [MeSH-major] Amyloid beta-Peptides / toxicity. Membrane Lipids / metabolism. Neuroblastoma / metabolism. Peptide Fragments / toxicity. Receptors, Nicotinic / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Membrane / metabolism. Cholesterol / metabolism. Dose-Response Relationship, Drug. Humans. Lipid Peroxidation / drug effects. Malondialdehyde / metabolism. Oxidative Stress / drug effects. Phospholipids / metabolism. Ubiquinone / metabolism. Vitamin E / metabolism. Vitamin E / pharmacology

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • Hazardous Substances Data Bank. MALONALDEHYDE .
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16608648.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Membrane Lipids; 0 / Peptide Fragments; 0 / Phospholipids; 0 / Receptors, Nicotinic; 0 / amyloid beta-protein (1-42); 0 / nicotinic receptor subunit alpha3; 1339-63-5 / Ubiquinone; 1406-18-4 / Vitamin E; 4Y8F71G49Q / Malondialdehyde; 97C5T2UQ7J / Cholesterol
  •  go-up   go-down


27. Billion K, Ibrahim H, Mauch C, Niessen CM: Increased soluble E-cadherin in melanoma patients. Skin Pharmacol Physiol; 2006;19(2):65-70
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, we did find a significant increase in serum E-cadherin levels of melanoma patients with advanced disease correlating with increased S100 tumor marker values, suggesting that increased cadherin shedding may contribute to melanoma progression.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Aspartic Acid Endopeptidases. Blotting, Western. Cell Line, Tumor. Endopeptidases / metabolism. Humans. S100 Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Melanoma.
  • 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
  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16685144.001).
  • [ISSN] 1660-5527
  • [Journal-full-title] Skin pharmacology and physiology
  • [ISO-abbreviation] Skin Pharmacol Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cadherins; 0 / S100 Proteins; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  •  go-up   go-down


28. Dowling P, O'Driscoll L, Meleady P, Henry M, Roy S, Ballot J, Moriarty M, Crown J, Clynes M: 2-D difference gel electrophoresis of the lung squamous cell carcinoma versus normal sera demonstrates consistent alterations in the levels of ten specific proteins. Electrophoresis; 2007 Dec;28(23):4302-10
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.
  • Proteins found to have increased abundance levels in squamous cell carcinoma sera compared to normal sera included apolipoprotein A-IV precursor, chain F; human complement component C3c, haptoglobin, serum amyloid A protein precursor and Ras-related protein Rab-7b.
  • [MeSH-major] Biomarkers, Tumor / blood. Blood Proteins / analysis. Carcinoma, Squamous Cell / blood. Electrophoresis, Gel, Two-Dimensional / methods. Lung Neoplasms / blood. Mass Spectrometry / methods

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • Genetic Alliance. consumer health - TEN.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18041032.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Haptoglobins
  •  go-up   go-down


29. Papassotiriou I, Alexiou VG, Tsironi M, Skenderi K, Spanos A, Falagas ME: Severe aseptic inflammation caused by long distance running (246 km) does not increase procalcitonin. Eur J Clin Invest; 2008 Apr;38(4):276-9
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.
  • Serum interleukin-6, serum amyloid A protein, C-reactive protein, tumour necrosis factor-alpha and procalcitonin concentrations were determined.
  • RESULTS: Serum interleukin-6, serum amyloid A protein and C-reactive protein were dramatically increased after the end of the race (150-, 116- and 10,470- fold increase of the mean values, respectively).
  • Tumour necrosis factor-alpha measurements revealed no significant changes.
  • [MeSH-minor] Adult. Humans. Interleukin-6 / metabolism. Middle Aged. Serum Amyloid A Protein / metabolism. Tumor Necrosis Factor-alpha / metabolism

  • Hazardous Substances Data Bank. Calcitonin .
  • 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
  • [CommentIn] Eur J Clin Invest. 2008 Oct;38(10):784-5 [18837805.001]
  • (PMID = 18339008.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Protein Precursors; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 56645-65-9 / procalcitonin; 9007-12-9 / Calcitonin; 9007-41-4 / C-Reactive Protein
  •  go-up   go-down


30. Kam AY, Tse TT, Kwan DH, Wong YH: Formyl peptide receptor like 1 differentially requires mitogen-activated protein kinases for the induction of glial fibrillary acidic protein and interleukin-1alpha in human U87 astrocytoma cells. Cell Signal; 2007 Oct;19(10):2106-17
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.
  • [MeSH-minor] Amyloid beta-Peptides / toxicity. Animals. Astrocytoma. CHO Cells. Cell Death. Cell Line, Tumor. Cricetinae. Cricetulus. Enzyme Inhibitors / pharmacology. GTP-Binding Protein alpha Subunits, Gi-Go / metabolism. Humans. Oligopeptides / pharmacology. Peptide Fragments / toxicity. Up-Regulation. src-Family Kinases / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 17643960.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Enzyme Inhibitors; 0 / FPR2 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Interleukin-1alpha; 0 / Oligopeptides; 0 / Peptide Fragments; 0 / Receptors, Formyl Peptide; 0 / Receptors, Lipoxin; 0 / Trp-Lys-Tyr-Met-Val-Met; 0 / amyloid beta-protein (1-42); EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go
  •  go-up   go-down


31. Iribarren P, Chen K, Hu J, Zhang X, Gong W, Wang JM: IL-4 inhibits the expression of mouse formyl peptide receptor 2, a receptor for amyloid beta1-42, in TNF-alpha-activated microglia. J Immunol; 2005 Nov 1;175(9):6100-6
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] IL-4 inhibits the expression of mouse formyl peptide receptor 2, a receptor for amyloid beta1-42, in TNF-alpha-activated microglia.
  • We have previously shown that TNF-alpha up-regulated the expression of formyl peptide receptor 2 (mFPR2) in mouse microglial cells, resulting in increased chemotactic responses of such cells to mFPR2 agonists, including amyloid beta1-42 (Abeta42), a critical pathogenic agent in Alzheimer's disease.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Interleukin-4 / pharmacology. Microglia / metabolism. Peptide Fragments / metabolism. Receptors, Formyl Peptide / antagonists & inhibitors. Tumor Necrosis Factor-alpha / antagonists & inhibitors

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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 = 16237106.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Receptors, Formyl Peptide; 0 / STAT6 Transcription Factor; 0 / Tumor Necrosis Factor-alpha; 0 / amyloid beta-protein (1-42); 0 / formyl peptide receptor 2, mouse; 207137-56-2 / Interleukin-4; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
  •  go-up   go-down


32. Akiyoshi T, Nakamura M, Yanai K, Nagai S, Wada J, Koga K, Nakashima H, Sato N, Tanaka M, Katano M: Gamma-secretase inhibitors enhance taxane-induced mitotic arrest and apoptosis in colon cancer cells. Gastroenterology; 2008 Jan;134(1):131-44
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.
  • BACKGROUND & AIMS: Colorectal cancers are resistant to conventional chemotherapeutic treatments, including taxanes. gamma-Secretase is a multimeric membrane protein complex responsible for the intramembrane proteolysis of various type I transmembrane proteins, including amyloid beta-precursor protein and Notch. gamma-Secretase inhibitors have attracted increasing interest as anticancer drugs because of their ability to inhibit Notch signaling.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Apoptosis / drug effects. Colonic Neoplasms / pathology. Enzyme Inhibitors / pharmacology. Mitosis / drug effects
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bridged Compounds / pharmacology. Cell Culture Techniques. Cell Line, Tumor. Humans. Taxoids / pharmacology. Vincristine / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VINCRISTINE .
  • 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 = 18166351.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bridged Compounds; 0 / Enzyme Inhibitors; 0 / Taxoids; 1605-68-1 / taxane; 5J49Q6B70F / Vincristine; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


33. Yerbury JJ, Wilson MR: Extracellular chaperones modulate the effects of Alzheimer's patient cerebrospinal fluid on Abeta(1-42) toxicity and uptake. Cell Stress Chaperones; 2010 Jan;15(1):115-21
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.
  • [MeSH-major] Alzheimer Disease / cerebrospinal fluid. Amyloid beta-Peptides / toxicity. Molecular Chaperones / pharmacology. Peptide Fragments / toxicity
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Line, Tumor. Humans. Male. Microscopy, Fluorescence. Middle Aged. Protein Binding

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • 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] Neurochem Int. 2006 Jun;48(8):718-28 [16490286.001]
  • [Cites] JAMA. 2000 Mar 22-29;283(12):1571-7 [10735393.001]
  • [Cites] J Neurochem. 1996 Sep;67(3):1324-7 [8752142.001]
  • [Cites] Stroke. 1996 Aug;27(8):1333-7 [8711797.001]
  • [Cites] J Cereb Blood Flow Metab. 2007 May;27(5):909-18 [17077814.001]
  • [Cites] J Neurochem. 1997 Jul;69(1):299-305 [9202323.001]
  • [Cites] J Biol Chem. 1997 Jul 25;272(30):18644-9 [9228033.001]
  • [Cites] J Neurochem. 1997 Nov;69(5):1904-11 [9349534.001]
  • [Cites] Biochemistry. 1997 Dec 9;36(49):15233-43 [9398251.001]
  • [Cites] FASEB J. 2007 Aug;21(10):2312-22 [17412999.001]
  • [Cites] J Neurochem. 2007 Oct;103(2):694-705 [17725582.001]
  • [Cites] Mol Biosyst. 2008 Jan;4(1):42-52 [18075673.001]
  • [Cites] Biochemistry. 2008 Jan 29;47(4):1176-85 [18171086.001]
  • [Cites] J Biol Chem. 2009 Feb 13;284(7):4246-54 [19074141.001]
  • [Cites] J Clin Invest. 2000 Dec;106(12):1489-99 [11120756.001]
  • [Cites] Biochemistry. 2000 Dec 26;39(51):15953-60 [11123922.001]
  • [Cites] J Biol Chem. 2001 Apr 13;276(15):11798-803 [11096092.001]
  • [Cites] J Neurochem. 2001 Jul;78(2):406-12 [11461976.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3693-8 [11739174.001]
  • [Cites] FEBS Lett. 2002 Feb 27;513(2-3):259-66 [11904161.001]
  • [Cites] Neurochem Int. 2002 Nov;41(5):345-52 [12176077.001]
  • [Cites] J Neurol. 2003 Mar;250(3):371-2; author reply 372 [12749328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10417-22 [12925731.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):631-9 [15295589.001]
  • [Cites] J Neuropathol Exp Neurol. 1981 Nov;40(6):592-612 [6795314.001]
  • [Cites] J Clin Invest. 1988 Jun;81(6):1858-64 [2454950.001]
  • [Cites] Lab Invest. 1992 Feb;66(2):223-30 [1370967.001]
  • [Cites] Ann Neurol. 1991 Oct;30(4):572-80 [1789684.001]
  • [Cites] J Immunol Methods. 1994 Jun 24;172(2):227-39 [7518485.001]
  • [Cites] Brain Res. 1995 Jul 10;685(1-2):211-6 [7583250.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3275-80 [9501253.001]
  • [Cites] Kidney Int. 1998 Jun;53(6):1647-53 [9607196.001]
  • [Cites] Psychiatry Clin Neurosci. 1998 Feb;52(1):107-10 [9682942.001]
  • [Cites] Arch Neurol. 1999 Feb;56(2):194-200 [10025424.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):6875-81 [10066740.001]
  • [Cites] Nat Rev Neurosci. 2005 Jan;6(1):11-22 [15611723.001]
  • [Cites] Int J Exp Pathol. 2005 Jun;86(3):147-59 [15910549.001]
  • [Cites] Biochemistry. 2005 Aug 16;44(32):10914-25 [16086594.001]
  • [Cites] Neurobiol Dis. 2005 Nov;20(2):233-40 [16242632.001]
  • [Cites] Pharmacol Ther. 2005 Nov;108(2):129-48 [16112736.001]
  • [Cites] EMBO Rep. 2005 Dec;6(12):1131-6 [16319958.001]
  • [Cites] Mech Ageing Dev. 2006 Feb;127(2):148-57 [16278007.001]
  • [Cites] Neuroreport. 1994 Apr 14;5(8):1012-4 [8061281.001]
  • [Cites] Trends Biochem Sci. 2000 Mar;25(3):95-8 [10694874.001]
  • [Cites] Brief Funct Genomic Proteomic. 2006 Jun;5(2):144-53 [16772279.001]
  • (PMID = 19472074.001).
  • [ISSN] 1466-1268
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Molecular Chaperones; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-42)
  • [Other-IDs] NLM/ PMC2866977
  •  go-up   go-down


34. Sevimli A, Misirlioğlu D, Yağci A, Bülbül A, Yilmaztepe A, Altunbas K: The role of chicken IL-1beta, IL-6 and TNF-alpha in the occurrence of amyloid arthropathy. Vet Res Commun; 2008 Oct;32(7):499-508
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 role of chicken IL-1beta, IL-6 and TNF-alpha in the occurrence of amyloid arthropathy.
  • In this study, the roles of IL-1beta, IL-6 and TNF-alpha in amyloid arthropathic chickens with variable amounts (severe, moderate and mild) of amyloid accumulation were investigated.
  • One hundred brown layer chicks were allocated into four groups and intra-articular injections of Freund's adjuvant were used to induce amyloid arthropathy in Groups II, III and IV.
  • At the end of the study, a positive correlation was observed among the incidence and severity of amyloidosis, the serum amyloid A levels and the IL-1beta values both in the serum and tissues.
  • [MeSH-major] Amyloidosis / veterinary. Interleukin-1beta / metabolism. Interleukin-6 / metabolism. Joint Diseases / veterinary. Poultry Diseases / metabolism. Tumor Necrosis Factor-alpha / metabolism

  • MedlinePlus Health Information. consumer health - Amyloidosis.
  • MedlinePlus Health Information. consumer health - Joint Disorders.
  • 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] Amyloid. 1998 Dec;5(4):266-78 [10036585.001]
  • [Cites] Microbiology. 2000 Dec;146 Pt 12:3217-26 [11101679.001]
  • [Cites] J Biol Chem. 1993 Dec 5;268(34):25624-31 [8244997.001]
  • [Cites] Brain Res Mol Brain Res. 1998 Aug 31;59(2):135-42 [9729336.001]
  • [Cites] Scand J Immunol. 1980;11(5):533-40 [6155692.001]
  • [Cites] Acta Neurol Scand. 1998 Jun;97(6):359-65 [9669467.001]
  • [Cites] J Biol Chem. 1987 Nov 15;262(32):15790-5 [2890635.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Oct;129(4):322-7 [8237250.001]
  • [Cites] Dev Comp Immunol. 2000 Jan;24(1):37-59 [10689097.001]
  • [Cites] Int J Parasitol. 1993 Aug;23(5):639-45 [8225766.001]
  • [Cites] Comp Immunol Microbiol Infect Dis. 2004 Jul;27(4):255-72 [15178000.001]
  • [Cites] J Burn Care Res. 2007 Jan-Feb;28(1):167-72 [17211221.001]
  • [Cites] Avian Pathol. 2005 Apr;34(2):143-9 [16191696.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Feb 6;314(2):363-9 [14733913.001]
  • [Cites] Lab Invest. 1996 Sep;75(3):371-5 [8804360.001]
  • [Cites] Poult Sci. 1995 Aug;74(8):1304-10 [7479508.001]
  • [Cites] J Rheumatol. 2004 Jun;31(6):1132-8 [15170926.001]
  • [Cites] Avian Dis. 1995 Oct-Dec;39(4):859-66 [8719221.001]
  • [Cites] Dev Comp Immunol. 1987 Spring;11(2):385-94 [3305105.001]
  • [Cites] Dev Comp Immunol. 2002 Oct;26(8):751-9 [12206838.001]
  • [Cites] Infect Immun. 2001 Apr;69(4):2527-34 [11254616.001]
  • [Cites] J Biol Chem. 1990 Apr 15;265(11):6318-22 [2156847.001]
  • [Cites] Clin Exp Immunol. 2001 Mar;123(3):408-11 [11298127.001]
  • [Cites] Mol Immunol. 2007 Jan;44(4):558-66 [16563507.001]
  • [Cites] Res Immunol. 1992 Sep;143(7):744-9 [1439148.001]
  • [Cites] Am J Kidney Dis. 2001 Feb;37(2):411-7 [11157384.001]
  • [Cites] Virus Res. 2005 Oct;113(1):44-50 [15893401.001]
  • [Cites] J Biol Chem. 1999 Feb 12;274(7):4300-8 [9933631.001]
  • [Cites] J Nutr. 1987 Sep;117(9):1629-37 [2443625.001]
  • [Cites] Dev Comp Immunol. 1999 Oct-Dec;23(7-8):629-40 [10579391.001]
  • [Cites] Res Immunol. 1992 Sep;143(7):755-9 [1439151.001]
  • [Cites] Dev Dyn. 1993 Nov;198(3):225-39 [8136526.001]
  • [Cites] J Bone Miner Res. 1999 Jul;14(7):1104-14 [10404010.001]
  • [Cites] Vet Immunol Immunopathol. 2000 Nov 23;77(1-2):55-69 [11068066.001]
  • [Cites] Scand J Immunol. 1996 Feb;43(2):210-8 [8633201.001]
  • [Cites] Vet Immunol Immunopathol. 2006 Nov 15;114(1-2):173-7 [16930722.001]
  • [Cites] J Immunol. 1991 Aug 15;147(4):1261-5 [1651357.001]
  • [Cites] J Invest Dermatol. 1989 Apr;92(4):605-10 [2539414.001]
  • [Cites] Vet Immunol Immunopathol. 2000 Aug 31;76(1-2):89-102 [10973688.001]
  • (PMID = 18612836.001).
  • [ISSN] 0165-7380
  • [Journal-full-title] Veterinary research communications
  • [ISO-abbreviation] Vet. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


35. Uberti D, Cenini G, Olivari L, Ferrari-Toninelli G, Porrello E, Cecchi C, Pensalfini A, Liguri G, Govoni S, Racchi M, Maurizio M: Over-expression of amyloid precursor protein in HEK cells alters p53 conformational state and protects against doxorubicin. J Neurochem; 2007 Oct;103(1):322-33
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] Over-expression of amyloid precursor protein in HEK cells alters p53 conformational state and protects against doxorubicin.
  • Here we show that human embryonic kidney (HEK) cells stably transfected with amyloid precursor protein (HEK-APP), expressed a conformational mutant-like and transcriptionally inactive p53 isoform, and turned out to be less sensitive to the cytotoxin doxorubicin in comparison with untransfected cells.
  • Changes in p53 conformational state and reduced sensitivity to doxorubicin were also found in untransfected HEK cells after exposure to nanomolar concentrations of beta-amyloid (Abeta) and these effects were antagonized by vitamin E.
  • [MeSH-major] Amyloid beta-Protein Precursor / biosynthesis. Doxorubicin / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Amyloid beta-Peptides / metabolism. Amyloid beta-Peptides / pharmacology. Antineoplastic Agents / pharmacology. Cell Line. Humans. Kidney / cytology. Kidney / drug effects. Kidney / metabolism. Peptide Fragments / metabolism. Peptide Fragments / pharmacology. Protein Conformation / drug effects. Protein Folding. Vitamin E / pharmacology

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Neurochem. 2008 Mar; 104(5) 1430. Pensafini, Anna [corrected to Pensalfini, Anna]
  • (PMID = 17608641.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / Antineoplastic Agents; 0 / Peptide Fragments; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 1406-18-4 / Vitamin E; 80168379AG / Doxorubicin
  •  go-up   go-down


36. Morel M, Couturier J, Pontcharraud R, Gil R, Fauconneau B, Paccalin M, Page G: Evidence of molecular links between PKR and mTOR signalling pathways in Abeta neurotoxicity: role of p53, Redd1 and TSC2. Neurobiol Dis; 2009 Oct;36(1):151-61
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.
  • This study analysed the crosslink between the up regulation of double-stranded RNA-dependent-protein kinase (PKR) and the down regulation of mammalian target of rapamycin (mTOR) signalling pathways via p53, the protein Regulated in the Development and DNA damage response 1 (Redd1) and the tuberous sclerosis complex (TSC2) factors in two beta-amyloid peptide (Abeta) neurotoxicity models.
  • [MeSH-major] Amyloid beta-Peptides / toxicity. Neurons / drug effects. Peptide Fragments / toxicity. Protein Kinases / metabolism. Signal Transduction / drug effects. Tumor Suppressor Proteins / metabolism. eIF-2 Kinase / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cells, Cultured. Cerebral Cortex / cytology. Cytoplasm / drug effects. Cytoplasm / metabolism. Embryo, Mammalian. Gene Expression Regulation / drug effects. Gene Expression Regulation / genetics. Humans. Immunoprecipitation / methods. Neuroblastoma / pathology. Phosphorylation / drug effects. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rats. Rats, Wistar. Repressor Proteins / genetics. Repressor Proteins / metabolism. TOR Serine-Threonine Kinases. Transfection / methods. Tumor Suppressor Protein p53 / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19631745.001).
  • [ISSN] 1095-953X
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / RNA, Small Interfering; 0 / RTP801 protein, rat; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / amyloid beta-protein (1-42); 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / eIF-2 Kinase
  •  go-up   go-down


37. Laforga JB, Aranda FI: Pseudoangiosarcomatous features in medullary thyroid carcinoma spindle-cell variant. Report of a case studied by FNA and immunohistochemistry. Diagn Cytopathol; 2007 Jul;35(7):424-8
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.
  • Microscopically, the tumor exhibited spindle-cell pattern intermingled with a striking angiosarcoma-like pattern characterized by the presence of abortive lumen and clefts containing erythrocytes.
  • Dense hyaline extracellular amyloid was present.
  • The tumor cells were strongly positive for cytokeratin, chromogranine-A, synaptophysine, serotonin, calcitonin, and CEA.
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Hemangiosarcoma / pathology. Humans. Male

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17580345.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


38. La Merrill M, Gordon RR, Hunter KW, Threadgill DW, Pomp D: Dietary fat alters pulmonary metastasis of mammary cancers through cancer autonomous and non-autonomous changes in gene expression. Clin Exp Metastasis; 2010 Feb;27(2):107-16
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.
  • Despite the substantial dietary impact on metastasis and its interaction with metastasis modifiers, HFD significantly altered the expression of only five genes in mammary tumors; four of which, including serum amyloid A (Saa), are downstream of the tumor suppressor PTEN.
  • Conversely, HFD altered the expression of 211 hepatic genes in a set of tumor free F2 control mice.
  • Independent of diet, pulmonary metastasis virulence correlates with mammary tumor expression of genes involved in endocrine cancers, inflammation, angiogenesis, and invasion.
  • These data support the existence of diet-dependent and independent cancer modifier networks underlying differential susceptibility to mammary cancer metastasis and suggest that diet influences cancer metastasis virulence through tumor autonomous and non-autonomous mechanisms.

  • MedlinePlus Health Information. consumer health - Dietary Fats.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • 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] Int J Cancer. 1998 Aug 12;77(4):640-4 [9679770.001]
  • [Cites] Oncogene. 2004 Aug 19;23(37):6304-15 [15318170.001]
  • [Cites] N Engl J Med. 2003 Apr 24;348(17):1625-38 [12711737.001]
  • [Cites] Ann Oncol. 2004 Jun;15(6):875-84 [15151943.001]
  • [Cites] Cancer Metastasis Rev. 1998 Mar;17(1):107-18 [9544426.001]
  • [Cites] Genome Biol. 2007;8(5):R76 [17493263.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6740-5 [17420468.001]
  • [Cites] Am J Physiol. 1996 May;270(5 Pt 1):L729-35 [8967506.001]
  • [Cites] Mutat Res. 2008 Sep-Oct;659(3):284-92 [18598780.001]
  • [Cites] J Lipid Res. 2003 Nov;44(11):2109-19 [12897189.001]
  • [Cites] Obes Rev. 2004 Aug;5(3):153-65 [15245384.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5679-84 [14522883.001]
  • [Cites] Breast Cancer Res Treat. 2007 May;102(3):253-61 [17031577.001]
  • [Cites] Br J Nutr. 2000 Oct;84(4):417-27 [11103212.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2008 Sep;20(9):843-54 [18794597.001]
  • [Cites] J Physiol. 2002 Dec 1;545(Pt 2):567-79 [12456835.001]
  • [Cites] Cancer Res. 2009 Jan 1;69(1):310-8 [19118016.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):169-79 [14729621.001]
  • [Cites] Oncogene. 2001 Aug 23;20(37):5093-9 [11526497.001]
  • [Cites] Br J Cancer. 2007 Apr 10;96(7):1092-100 [17353919.001]
  • [Cites] Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261.001]
  • [Cites] Int J Cardiol. 1998 Jul 1;65(2):139-47 [9706808.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):96-102 [12794763.001]
  • [Cites] Bioinformatics. 2002 Feb;18(2):339-40 [11847090.001]
  • [Cites] Oncogene. 2000 Jan 13;19(2):241-7 [10645002.001]
  • [Cites] Arch Physiol Biochem. 1995 Dec;103(6):715-9 [8697004.001]
  • [Cites] J Proteome Res. 2008 Nov;7(11):4775-83 [18828625.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jul;80(1):87-97 [12889602.001]
  • [Cites] Cancer. 2007 Jun 15;109(12 Suppl):2712-49 [17503428.001]
  • [Cites] Angiogenesis. 1999;3(3):221-9 [14517421.001]
  • [Cites] Mol Cell Proteomics. 2007 Apr;6(4):575-88 [17220478.001]
  • [Cites] Nat Cell Biol. 2008 Nov;10(11):1349-55 [18820689.001]
  • [Cites] J Biol Chem. 2001 Jul 27;276(30):28443-50 [11328805.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):765-70 [17429393.001]
  • [Cites] FASEB J. 2007 Dec;21(14):3994-4004 [17625068.001]
  • [Cites] Biosci Biotechnol Biochem. 2008 Jan;72(1):70-81 [18175929.001]
  • [Cites] Endocr Relat Cancer. 2007 Dec;14(4):1021-8 [18045953.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2009 Jan;296(1):E203-10 [18840765.001]
  • [Cites] Bioinformatics. 2008 Jul 1;24(13):1547-8 [18467348.001]
  • [Cites] Genetics. 1994 Nov;138(3):963-71 [7851788.001]
  • [Cites] Mamm Genome. 2008 Mar;19(3):179-89 [18288525.001]
  • [Cites] Nat Genet. 2007 Aug;39(8):1025-32 [17632513.001]
  • [Cites] Oncogene. 2005 Jul 14;24(30):4851-60 [15897904.001]
  • [Cites] Am J Respir Cell Mol Biol. 1994 Nov;11(5):625-30 [7524568.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5973-81 [15342376.001]
  • [Cites] Mamm Genome. 2008 Mar;19(3):163-78 [18286334.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):279-92 [16728564.001]
  • [Cites] Hepatology. 2005 May;41(5):1074-84 [15841469.001]
  • [Cites] Genes Dev. 1998 Feb 15;12(4):502-13 [9472019.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2009 Jan;296(1):E157-64 [19001549.001]
  • (PMID = 20151316.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / 5T32 HD049311; United States / NIDDK NIH HHS / DK / DK056350; United States / NIEHS NIH HHS / ES / T32ES007126; United States / NCI NIH HHS / CA / U01CA105417; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BTN1A1 protein, human; 0 / Btn1a1 protein, mouse; 0 / Butyrophilins; 0 / Dietary Fats; 0 / Membrane Glycoproteins
  •  go-up   go-down


39. Jimenez Del Rio M, Velez-Pardo C: Insulin-like growth factor-1 prevents Abeta[25-35]/(H2O2)- induced apoptosis in lymphocytes by reciprocal NF-kappaB activation and p53 inhibition via PI3K-dependent pathway. Growth Factors; 2006 Mar;24(1):67-78
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.
  • [MeSH-major] Amyloid beta-Peptides / physiology. Apoptosis. Hydrogen Peroxide / metabolism. Insulin-Like Growth Factor I / physiology. Lymphocytes / physiology. NF-kappa B / metabolism. Peptide Fragments / physiology. Phosphatidylinositol 3-Kinases / metabolism. Tumor Suppressor Protein p53 / antagonists & inhibitors

  • Hazardous Substances Data Bank. TOLUENE .
  • Hazardous Substances Data Bank. (L)-PROLINE .
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 16393695.001).
  • [ISSN] 0897-7194
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Benzothiazoles; 0 / Chromones; 0 / Morpholines; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Thiazoles; 0 / Thiocarbamates; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (25-35); 0 / pifithrin; 135467-92-4 / prolinedithiocarbamate; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 3FPU23BG52 / Toluene; 67763-96-6 / Insulin-Like Growth Factor I; 9DLQ4CIU6V / Proline; BBX060AN9V / Hydrogen Peroxide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  •  go-up   go-down


40. Kip KE, Marroquin OC, Shaw LJ, Arant CB, Wessel TR, Olson MB, Johnson BD, Mulukutla S, Sopko G, Merz CN, Reis SE: Global inflammation predicts cardiovascular risk in women: a report from the Women's Ischemia Syndrome Evaluation (WISE) study. Am Heart J; 2005 Nov;150(5):900-6
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.
  • METHODS: From the WISE study, 580 women with fasting plasma samples of inflammatory markers (interleukin [IL]-6, IL-18, tumor necrosis factor alpha, transforming growth factor beta, CRP, serum amyloid A [SAA], and intercellular adhesion molecules) were analyzed over a median of 4.7 years follow-up.
  • RESULTS: In factor analysis, a "proinflammation" factor (cluster) loaded on IL-6, CRP, and SAA (r = 0.63-0.87); a "proinflammation and anti-inflammation" cluster loaded on IL-18 and tumor necrosis factor alpha (r = 0.72, 0.77); and an "immunosuppressive" factor loaded singly on transforming growth factor beta (r = 0.96).

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • 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 = 16290958.001).
  • [ISSN] 1097-6744
  • [Journal-full-title] American heart journal
  • [ISO-abbreviation] Am. Heart J.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HV / N01-HV-68161; United States / NHLBI NIH HHS / HV / N01-HV-68162; United States / NHLBI NIH HHS / HV / N01-HV-68163; United States / NHLBI NIH HHS / HV / N01-HV-68164; United States / NHLBI NIH HHS / HL / R01-HL-073412-01; United States / NHLBI NIH HHS / HL / U01 HL649141; United States / NHLBI NIH HHS / HL / U01 HL649241; United States / PHS HHS / / U0164829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inflammation Mediators
  •  go-up   go-down


41. Nehar S, Mishra M, Heese K: Identification and characterisation of the novel amyloid-beta peptide-induced protein p17. FEBS Lett; 2009 Oct 6;583(19):3247-53
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 and characterisation of the novel amyloid-beta peptide-induced protein p17.
  • Amyloid-beta peptide (Abeta) achieves neurodegeneration through unknown mechanisms.
  • It impedes survival factors and enhances amyloid precursor protein expression thus suggesting its involvement in the Abeta-mediated pro-apoptotic pathways in AD.
  • [MeSH-major] Alzheimer Disease / metabolism. Alzheimer Disease / pathology. Amyloid beta-Peptides / metabolism. Apoptosis. Apoptosis Regulatory Proteins / metabolism. Peptide Fragments / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Disease Models, Animal. Humans. Mice. Molecular Sequence Data. Rats. Tissue Distribution


42. Gopalakrishnan R, Simonton S, Rohrer MD, Koutlas IG: Cystic variant of calcifying epithelial odontogenic tumor. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2006 Dec;102(6):773-7
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] Cystic variant of calcifying epithelial odontogenic tumor.
  • Calcifying epithelial odontogenic tumor (CEOT) is a benign, locally aggressive odontogenic neoplasm characterized by sheets and nests of epithelial cells with deeply eosinophilic or occasionally clear cytoplasm, calcifications, and eosinophilic amorphous material that stains positive for amyloid.

  • Genetic Alliance. consumer health - Calcifying Epithelial Odontogenic Tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17138180.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


43. Costantini C, Weindruch R, Della Valle G, Puglielli L: A TrkA-to-p75NTR molecular switch activates amyloid beta-peptide generation during aging. Biochem J; 2005 Oct 1;391(Pt 1):59-67
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] A TrkA-to-p75NTR molecular switch activates amyloid beta-peptide generation during aging.
  • The abnormal accumulation of Abeta (amyloid beta-peptide) in the form of senile plaques is one of the main characteristics of AD.
  • In the present study, we show that two members of the neurotrophin receptor superfamily, TrkA (tyrosine kinase receptor A) and p75NTR (p75 neurotrophin receptor), differentially regulate the processing of APP (amyloid precursor protein): TrkA reduces, whereas p75NTR activates, beta-cleavage of APP.

  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 1999 Oct 1;19(19):8199-206 [10493721.001]
  • [Cites] Nat Neurosci. 2003 Apr;6(4):345-51 [12658281.001]
  • [Cites] J Clin Invest. 1999 Nov;104(9):1171-3 [10545515.001]
  • [Cites] Cancer Res. 2000 Feb 1;60(3):650-6 [10676649.001]
  • [Cites] Exp Neurol. 2000 Jan;161(1):245-58 [10683291.001]
  • [Cites] Trends Pharmacol Sci. 2000 May;21(5):161-3 [10785643.001]
  • [Cites] J Cell Sci. 2000 Jun;113 ( Pt 11):1857-70 [10806097.001]
  • [Cites] Nat Neurosci. 2001 Mar;4(3):231-2 [11224535.001]
  • [Cites] Nat Neurosci. 2001 Mar;4(3):233-4 [11224536.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1769-77 [11297616.001]
  • [Cites] J Neurosci. 2001 Jul 15;21(14):5121-9 [11438587.001]
  • [Cites] Mol Cell Neurosci. 2001 Aug;18(2):210-20 [11520181.001]
  • [Cites] Nat Neurosci. 2001 Oct;4(10):977-8 [11559852.001]
  • [Cites] Nat Cell Biol. 2001 Oct;3(10):905-12 [11584272.001]
  • [Cites] Science. 2001 Nov 30;294(5548):1945-8 [11729324.001]
  • [Cites] J Biol Chem. 2003 May 30;278(22):19777-83 [12649271.001]
  • [Cites] J Neurosci. 2003 Aug 13;23(19):7385-94 [12917374.001]
  • [Cites] Am J Pathol. 2004 Feb;164(2):719-25 [14742275.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2070-5 [14970312.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):20539-45 [14871891.001]
  • [Cites] Science. 2004 May 7;304(5672):833-4 [15131296.001]
  • [Cites] Nature. 2004 Jun 24;429(6994):883-91 [15190254.001]
  • [Cites] Mol Psychiatry. 2004 Jul;9(7):664-83 [15052274.001]
  • [Cites] J Neurosci Res. 2004 Aug 15;77(4):465-74 [15264216.001]
  • [Cites] Ann Neurol. 2004 Oct;56(4):520-31 [15455399.001]
  • [Cites] EMBO Rep. 2004 Sep;5(9):867-71 [15470383.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):569-73 [1309947.001]
  • [Cites] Cell. 1992 May 29;69(5):737-49 [1317267.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10703-6 [7938014.001]
  • [Cites] J Biol Chem. 1995 Dec 22;270(51):30701-8 [8530509.001]
  • [Cites] Oncogene. 1997 Mar 27;14(12):1463-70 [9136990.001]
  • [Cites] N Engl J Med. 1997 Oct 2;337(14):986-94 [9309105.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2333-40 [9410912.001]
  • [Cites] Neurosci Lett. 1998 Jan 30;241(2-3):151-4 [9507943.001]
  • [Cites] Ann N Y Acad Sci. 1998 Jun 19;845:32-45 [9668341.001]
  • [Cites] Trends Neurosci. 1998 Oct;21(10):438-44 [9786342.001]
  • [Cites] Brain Res Mol Brain Res. 1999 May 21;69(1):21-34 [10350634.001]
  • [Cites] J Comp Neurol. 1999 Aug 2;410(3):368-86 [10404406.001]
  • [Cites] Biochim Biophys Acta. 1999 Jul 30;1439(2):291-8 [10425402.001]
  • [Cites] Science. 1999 Aug 27;285(5432):1390-3 [10464095.001]
  • [Cites] Chembiochem. 2001 Feb 2;2(2):141-3 [11828438.001]
  • [Cites] Ann Neurol. 2002 Jun;51(6):783-6 [12112088.001]
  • [Cites] Arch Neurol. 2002 Sep;59(9):1381-9 [12223024.001]
  • [Cites] J Neurochem. 2002 Aug;82(4):809-18 [12358786.001]
  • [Cites] Nat Neurosci. 2002 Nov;5(11):1131-6 [12404007.001]
  • [Cites] Exp Neurol. 2002 Nov;178(1):104-11 [12460612.001]
  • [Cites] Neurobiol Aging. 1999 Mar-Apr;20(2):157-65 [10537025.001]
  • (PMID = 15966860.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS045669; United States / NINDS NIH HHS / NS / NS045669
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Ceramides; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Receptor, Nerve Growth Factor; 52665-74-4 / manumycin; EC 2.7.10.1 / Receptor, trkA
  • [Other-IDs] NLM/ PMC1237139
  •  go-up   go-down


44. Schmid K, Haslbeck M, Buchner J, Somoza V: Induction of heat shock proteins and the proteasome system by casein-N epsilon-(carboxymethyl)lysine and N epsilon-(carboxymethyl)lysine in Caco-2 cells. Ann N Y Acad Sci; 2008 Apr;1126:257-61
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.
  • Exposure of Caco-2 cells to beta-amyloid, a nonglycation product, revealed similar results.
  • [MeSH-minor] Adenocarcinoma / metabolism. Blotting, Western. Cell Line, Tumor. Colonic Neoplasms / metabolism. Humans. Mass Spectrometry. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

  • Hazardous Substances Data Bank. L-Lysine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18448826.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caseins; 0 / Glycosylation End Products, Advanced; 5746-04-3 / N(6)-carboxymethyllysine; K3Z4F929H6 / Lysine
  •  go-up   go-down


45. Wen Y, Yu WH, Maloney B, Bailey J, Ma J, Marié I, Maurin T, Wang L, Figueroa H, Herman M, Krishnamurthy P, Liu L, Planel E, Lau LF, Lahiri DK, Duff K: Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing. Neuron; 2008 Mar 13;57(5):680-90
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] Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing.
  • Cyclin-dependent kinase 5 (cdk5) has been implicated in Alzheimer's disease (AD) pathogenesis.
  • Here, we demonstrate that overexpression of p25, an activator of cdk5, led to increased levels of BACE1 mRNA and protein in vitro and in vivo.
  • A p25/cdk5 responsive region containing multiple sites for signal transducer and activator of transcription (STAT1/3) was identified in the BACE1 promoter.
  • STAT3 interacts with the BACE1 promoter, and p25-overexpressing mice had elevated levels of pSTAT3 and BACE1, whereas cdk5-deficient mice had reduced levels.
  • Furthermore, mice with a targeted mutation in the STAT3 cdk5 responsive site had lower levels of BACE1.
  • Increased BACE levels in p25 overexpressing mice correlated with enhanced amyloidogenic processing that could be reversed by a cdk5 inhibitor.
  • These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis.

  • 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).
  • 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 CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEBS Lett. 2002 Jul 17;523(1-3):58-62 [12123804.001]
  • [Cites] Arch Neurol. 2002 Sep;59(9):1381-9 [12223024.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Dec 6;299(3):373-6 [12445809.001]
  • [Cites] Nat Med. 2003 Jan;9(1):3-4 [12514700.001]
  • [Cites] Neuron. 2003 Apr 10;38(1):33-46 [12691662.001]
  • [Cites] Nat Cell Biol. 2003 May;5(5):486-8 [12679784.001]
  • [Cites] Nature. 2003 May 22;423(6938):435-9 [12761548.001]
  • [Cites] J Neurochem. 2003 Aug;86(3):572-81 [12859671.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Aug 8;307(4):922-7 [12878199.001]
  • [Cites] Brain Res Mol Brain Res. 2003 Aug 19;116(1-2):155-8 [12941471.001]
  • [Cites] Cell. 2003 Aug 22;114(4):469-82 [12941275.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):34026-34 [12826674.001]
  • [Cites] Nat Neurosci. 2003 Oct;6(10):1039-47 [14502288.001]
  • [Cites] J Cell Biol. 2003 Oct 13;163(1):83-95 [14557249.001]
  • [Cites] J Cell Biol. 2003 Nov 24;163(4):813-24 [14623869.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(1):407-19 [14673173.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):865-74 [14701757.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3632-7 [14978286.001]
  • [Cites] Brain Res. 2004 May 29;1009(1-2):1-8 [15120577.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 5;103(49):18727-32 [17121991.001]
  • [Cites] PLoS One. 2006;1:e51 [17183681.001]
  • [Cites] J Neurosci. 2007 Feb 21;27(8):1981-91 [17314294.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6728-33 [15096606.001]
  • [Cites] EMBO Rep. 2004 Jun;5(6):620-5 [15167888.001]
  • [Cites] FASEB J. 2004 Jun;18(9):1034-6 [15059975.001]
  • [Cites] FASEB J. 2004 Jun;18(9):1037-9 [15059977.001]
  • [Cites] Curr Opin Neurobiol. 2004 Jun;14(3):390-4 [15194121.001]
  • [Cites] J Cell Sci. 2004 Sep 15;117(Pt 20):4739-48 [15331630.001]
  • [Cites] FASEB J. 2004 Oct;18(13):1571-3 [15289451.001]
  • [Cites] FEBS Lett. 1993 Dec 6;335(2):171-5 [8253190.001]
  • [Cites] FEBS Lett. 1993 Dec 28;336(3):417-24 [8282104.001]
  • [Cites] J Biol Chem. 1994 May 27;269(21):15253-7 [8195161.001]
  • [Cites] Nature. 1994 Sep 29;371(6496):419-23 [8090221.001]
  • [Cites] J Biol Chem. 1994 Dec 9;269(49):30981-7 [7983034.001]
  • [Cites] Neuroreport. 1995 Feb 15;6(3):477-80 [7766847.001]
  • [Cites] J Biol Chem. 1996 Aug 30;271(35):21108-13 [8702879.001]
  • [Cites] Science. 1996 Oct 4;274(5284):99-102 [8810256.001]
  • [Cites] J Biol Chem. 2005 Sep 16;280(37):32499-504 [16033761.001]
  • [Cites] Neurosci Res. 2006 Jan;54(1):24-9 [16290302.001]
  • [Cites] J Interferon Cytokine Res. 2005 Dec;25(12):733-44 [16375601.001]
  • [Cites] Curr Mol Med. 2006 Feb;6(1):119-33 [16472119.001]
  • [Cites] J Mol Neurosci. 2006;29(1):65-80 [16757811.001]
  • [Cites] J Mol Neurosci. 2006;29(1):81-99 [16757812.001]
  • [Cites] J Neurosci. 2006 Oct 11;26(41):10536-41 [17035538.001]
  • [Cites] FEBS Lett. 2006 Dec 11;580(28-29):6550-60 [17113083.001]
  • [Cites] Biochim Biophys Acta. 2007 Apr;1772(4):473-83 [17113760.001]
  • [Cites] J Neurosci. 2007 Apr 4;27(14):3639-49 [17409228.001]
  • [Cites] Brain Res. 2007 Aug 3;1161:116-23 [17586478.001]
  • [Cites] J Biol Chem. 2007 Oct 26;282(43):31460-8 [17726017.001]
  • [Cites] Science. 1999 Oct 22;286(5440):735-41 [10531052.001]
  • [Cites] Nature. 1999 Dec 9;402(6762):615-22 [10604467.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2910-5 [10706614.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11173-8 [8855328.001]
  • [Cites] J Cereb Blood Flow Metab. 1996 Nov;16(6):1219-23 [8898694.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Feb;56(2):165-70 [9034370.001]
  • [Cites] JAMA. 1997 Mar 12;277(10):813-7 [9052711.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 1;25(11):2062-7 [9153303.001]
  • [Cites] Nature. 1998 Jan 22;391(6665):387-90 [9450754.001]
  • [Cites] Biochem Mol Biol Int. 1998 Nov;46(4):755-64 [9844737.001]
  • [Cites] Neurosci Res. 1999 May;34(1):21-9 [10413323.001]
  • [Cites] J Med Chem. 2004 Dec 16;47(26):6447-50 [15588077.001]
  • [Cites] J Neurochem. 2005 Feb;92(3):628-36 [15659232.001]
  • [Cites] J Cell Sci. 2005 Mar 15;118(Pt 6):1291-8 [15741232.001]
  • [Cites] Neurobiol Aging. 2005 Aug-Sep;26(8):1167-75 [15917100.001]
  • [Cites] Methods Mol Biol. 2005;299:267-78 [15980611.001]
  • [Cites] Methods Mol Biol. 2005;299:279-97 [15980612.001]
  • [Cites] Mol Cell Biol. 2006 May;26(9):3353-64 [16611980.001]
  • [Cites] Glia. 2000 May;30(3):253-70 [10756075.001]
  • [Cites] Nature. 2000 May 18;405(6784):360-4 [10830966.001]
  • [Cites] Neurobiol Aging. 2000 Mar-Apr;21(2):321-30 [10867217.001]
  • [Cites] J Biol Chem. 2000 Oct 6;275(40):30849-54 [10801872.001]
  • [Cites] J Biol Chem. 2000 Oct 27;275(43):33729-37 [10924510.001]
  • [Cites] Neuron. 2000 Dec;28(3):681-96 [11163259.001]
  • [Cites] Eur J Neurosci. 2001 Jan;13(2):241-7 [11168528.001]
  • [Cites] Nat Neurosci. 2001 Mar;4(3):231-2 [11224535.001]
  • [Cites] Eur J Biochem. 2001 Mar;268(6):1518-27 [11248668.001]
  • [Cites] Nat Neurosci. 2001 Apr;4(4):374-81 [11276227.001]
  • [Cites] J Biol Chem. 2001 May 4;276(18):14634-41 [11278841.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Oct;2(10):749-59 [11584302.001]
  • [Cites] Brain Res. 2001 Nov 16;919(1):115-21 [11689168.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45443-55 [11579100.001]
  • [Cites] Mol Cell Neurosci. 2002 Feb;19(2):175-85 [11860271.001]
  • [Cites] Ann Neurol. 2002 Jun;51(6):783-6 [12112088.001]
  • (PMID = 18341989.001).
  • [ISSN] 1097-4199
  • [Journal-full-title] Neuron
  • [ISO-abbreviation] Neuron
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG18379; United States / NIA NIH HHS / AG / R01 AG018884; United States / NIA NIH HHS / AG / P01 AG017216-020004; United States / NINDS NIH HHS / NS / NS48447; United States / NIA NIH HHS / AG / AG017216-020004; United States / NINDS NIH HHS / NS / P01 NS048447; United States / NINDS NIH HHS / NS / NS048447-030005; United States / NIA NIH HHS / AG / AG18884; United States / NINDS NIH HHS / NS / P01 NS048447-030005; United States / NIA NIH HHS / AG / P01 AG017216; United States / NIA NIH HHS / AG / R01 AG018379; United States / NIA NIH HHS / AG / AG172116
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / Cdk5r1 protein, mouse; 0 / Nerve Tissue Proteins; EC 2.7.- / Phosphotransferases; EC 2.7.11.22 / Cyclin-Dependent Kinase 5; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS43369; NLM/ PMC2329816
  •  go-up   go-down


46. Kusaka T, Ueno M, Miki T, Kanenishi K, Nagai Y, Huang CL, Okamoto Y, Ogawa T, Onodera M, Itoh S, Akiguchi I, Sakamoto H: Accumulation of triosephosphate isomerase, with sequence homology to Beta amyloid peptides, in vessel walls of the newborn piglet hippocampus. Microsc Res Tech; 2007 Jul;70(7):648-55
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] Accumulation of triosephosphate isomerase, with sequence homology to Beta amyloid peptides, in vessel walls of the newborn piglet hippocampus.
  • We investigated whether beta-amyloid (Abeta)-like immunoreactivity was seen in the brains of newborn piglets.
  • It was colocalized with immunoreactivity for receptor for advanced glycation end product and tumor necrosis factor-alpha.
  • [MeSH-major] Amyloid beta-Peptides / chemistry. Blood Vessels / enzymology. Hippocampus / blood supply. Hippocampus / enzymology. Triose-Phosphate Isomerase / chemistry. Triose-Phosphate Isomerase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17393492.001).
  • [ISSN] 1059-910X
  • [Journal-full-title] Microscopy research and technique
  • [ISO-abbreviation] Microsc. Res. Tech.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; EC 5.3.1.1 / Triose-Phosphate Isomerase
  •  go-up   go-down


47. Choi SC, Choi EJ, Oh HM, Lee S, Lee JK, Lee MS, Shin YI, Choi SJ, Chae JR, Lee KM, Lee WJ, Park JS, Shin CY, Oh TY, Jun CD: DA-9601, a standardized extract of Artemisia asiatica, blocks TNF-alpha-induced IL-8 and CCL20 production by inhibiting p38 kinase and NF-kappaB pathways in human gastric epithelial cells. World J Gastroenterol; 2006 Aug 14;12(30):4850-8
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.
  • [MeSH-major] Chemokines, CC / metabolism. Epithelial Cells / metabolism. Interleukin-8 / metabolism. Macrophage Inflammatory Proteins / metabolism. NF-kappa B / antagonists & inhibitors. Plant Extracts / pharmacology. Tumor Necrosis Factor-alpha / metabolism. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

  • 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] FEBS Lett. 1983 Jul 11;158(1):41-4 [6407870.001]
  • [Cites] J Immunol. 2004 Jun 1;172(11):7069-77 [15153529.001]
  • [Cites] Mol Cell Biol. 1994 Dec;14(12):8376-84 [7969172.001]
  • [Cites] Science. 1994 Dec 9;266(5191):1719-23 [7992057.001]
  • [Cites] J Biol Chem. 1995 Mar 31;270(13):7420-6 [7535770.001]
  • [Cites] J Biol Chem. 1997 Jan 31;272(5):2753-61 [9006914.001]
  • [Cites] Infect Immun. 1997 Feb;65(2):843-6 [9009355.001]
  • [Cites] J Biol Chem. 1997 Feb 28;272(9):5846-53 [9038201.001]
  • [Cites] Infect Immun. 1997 Sep;65(9):3622-30 [9284128.001]
  • [Cites] Br Med Bull. 1998;54(1):139-50 [9604438.001]
  • [Cites] Pancreas. 1998 Aug;17(2):153-7 [9700946.001]
  • [Cites] Arch Pharm Res. 1998 Oct;21(5):508-13 [9875486.001]
  • [Cites] J Clin Invest. 1999 Mar;103(6):851-8 [10079106.001]
  • [Cites] Am J Physiol Cell Physiol. 2000 Mar;278(3):C451-62 [10712233.001]
  • [Cites] Blood. 2000 May 15;95(10):3044-51 [10807767.001]
  • [Cites] Free Radic Res. 2000 Dec;33(6):785-94 [11237100.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Apr;280(4):G710-9 [11254498.001]
  • [Cites] Free Radic Biol Med. 2001 Apr 15;30(8):905-15 [11295533.001]
  • [Cites] Eur J Immunol. 2001 Jul;31(7):1981-8 [11449350.001]
  • [Cites] Mutat Res. 2001 Sep 1;480-481:189-200 [11506813.001]
  • [Cites] Gut. 2001 Sep;49(3):364-71 [11511558.001]
  • [Cites] Mutat Res. 2001 Sep 20;496(1-2):191-8 [11551495.001]
  • [Cites] Amyloid. 2001 Sep;8(3):194-201 [11676296.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13722-7 [11717433.001]
  • [Cites] FEBS Lett. 2001 Dec 14;509(3):439-45 [11749970.001]
  • [Cites] Int Immunol. 2002 Feb;14(2):147-55 [11809734.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):7713-9 [11756416.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 Jul;283(1):C31-41 [12055070.001]
  • [Cites] Int J Cancer. 2002 Aug 1;100(4):456-62 [12115530.001]
  • [Cites] Infect Immun. 2003 Apr;71(4):2153-62 [12654837.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Oct;14(5):409-26 [12948524.001]
  • [Cites] J Ethnopharmacol. 2003 Oct;88(2-3):269-73 [12963154.001]
  • [Cites] Infect Immun. 1993 Feb;61(2):602-9 [8423089.001]
  • (PMID = 16937467.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CCL20 protein, human; 0 / Chemokine CCL20; 0 / Chemokines, CC; 0 / DA 9601; 0 / Enzyme Inhibitors; 0 / Interleukin-8; 0 / Macrophage Inflammatory Proteins; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC4087619
  •  go-up   go-down


48. Laskowitz DT, Song P, Wang H, Mace B, Sullivan PM, Vitek MP, Dawson HN: Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic. J Neurotrauma; 2010 Nov;27(11):1983-95
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.
  • We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele.
  • [MeSH-minor] Amyloid beta-Peptides / metabolism. Animals. Blotting, Western. Brain / pathology. Cytokines / biosynthesis. Enzyme-Linked Immunosorbent Assay. Gliosis / pathology. Humans. Immunohistochemistry. Male. Mice. Mice, Transgenic. Motor Activity / physiology. Platelet-Derived Growth Factor / genetics. Polymorphism, Genetic / genetics. Psychomotor Performance / physiology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Necrosis Factor-alpha / metabolism. tau Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Degenerative Nerve Diseases.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • 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 = 20812776.001).
  • [ISSN] 1557-9042
  • [Journal-full-title] Journal of neurotrauma
  • [ISO-abbreviation] J. Neurotrauma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Apolipoproteins E; 0 / Cytokines; 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / tau Proteins
  •  go-up   go-down


49. Henriques AG, Vieira SI, Crespo-López ME, Guiomar de Oliveira MA, da Cruz e Silva EF, da Cruz e Silva OA: Intracellular sAPP retention in response to Abeta is mapped to cytoskeleton-associated structures. J Neurosci Res; 2009 May 1;87(6):1449-61
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.
  • Amyloid beta (Abeta) contributes to neurodegeneration in Alzheimer's disease and provides a close association between molecular events and pathology, although the underlying molecular mechanisms are unclear.
  • In the work described here, Abeta did not induce amyloid precursor protein (APP) expression, but APP processing/trafficking was markedly affected.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Amyloid beta-Protein Precursor / metabolism. Cytoskeleton / metabolism. Neurons / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Northern. COS Cells. Cell Line. Cell Line, Tumor. Cercopithecus aethiops. Gene Expression. Immunohistochemistry. PC12 Cells. RNA / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19105196.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 63231-63-0 / RNA
  •  go-up   go-down


50. Cenini G, Cecchi C, Pensalfini A, Bonini SA, Ferrari-Toninelli G, Liguri G, Memo M, Uberti D: Generation of reactive oxygen species by beta amyloid fibrils and oligomers involves different intra/extracellular pathways. Amino Acids; 2010 Apr;38(4):1101-6
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] Generation of reactive oxygen species by beta amyloid fibrils and oligomers involves different intra/extracellular pathways.
  • A neuropathological characteristic of Alzheimer's disease is the extracellular accumulation of amyloid beta peptide (Abeta) in neuritic plaques.
  • [MeSH-major] Alzheimer Disease / physiopathology. Amyloid / metabolism. Amyloid beta-Peptides / metabolism. Peptide Fragments / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Adsorption / drug effects. Biological Transport / drug effects. Cell Line, Tumor. Cell Membrane / metabolism. Cell Survival / drug effects. Colchicine / pharmacology. Cytoskeleton / drug effects. Cytosol / metabolism. Endocytosis / drug effects. Humans. Intracellular Membranes / metabolism. Microscopy, Confocal. Neurons / drug effects. Neurons / pathology

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • Hazardous Substances Data Bank. COLCHICINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Amino Acids. 2010 Apr;38(4):1107. Giovanna, Cenini [corrected to Cenini, Giovanna]
  • (PMID = 19582548.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Amyloid; 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / Reactive Oxygen Species; 0 / amyloid beta-protein (1-42); SML2Y3J35T / Colchicine
  •  go-up   go-down


51. Cavallaro RA, Fuso A, D'Anselmi F, Seminara L, Scarpa S: The effect of S-adenosylmethionine on CNS gene expression studied by cDNA microarray analysis. J Alzheimers Dis; 2006 Aug;9(4):415-9
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.
  • It has already been shown that DNA methylation is involved in amyloid-beta-protein precursor (AbetaPP) processing and amyloid-beta(Abeta) production through the regulation of Presenilin 1 (PS1) expression and that exogenous SAM can silence the gene reducing Abeta.
  • [MeSH-minor] Aging. Amyloid beta-Protein Precursor / drug effects. Cell Line, Tumor / pathology. Chromatography, High Pressure Liquid. DNA Methylation / drug effects. Humans. Membrane Proteins / drug effects. Membrane Proteins / metabolism. Neuroblastoma / metabolism. Neuroblastoma / pathology. Presenilin-1. RNA / drug effects. RNA / genetics. RNA / metabolism

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16917150.001).
  • [ISSN] 1387-2877
  • [Journal-full-title] Journal of Alzheimer's disease : JAD
  • [ISO-abbreviation] J. Alzheimers Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Membrane Proteins; 0 / PSEN1 protein, human; 0 / Presenilin-1; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
  •  go-up   go-down


52. Zahradník FJ: Quantitative analysis of streptococcal exoprotein flow to the host receptor--exact basis for therapy of tumors and Alzheimer's disease. Folia Microbiol (Praha); 2005;50(1):63-9
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.
  • [MeSH-minor] Alzheimer Disease / drug therapy. Alzheimer Disease / metabolism. Amyloid beta-Peptides / metabolism. Bacterial Proteins / metabolism. Biomarkers, Tumor / metabolism. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Neoplasms / drug therapy. Neoplasms / metabolism. Peptides / metabolism. Protein Binding

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 1980 Jan 31;283(5746):433-8 [7352023.001]
  • [Cites] Anticancer Res. 1994 Nov-Dec;14(6B):2819-25 [7872725.001]
  • [Cites] Transplant Rev. 1974;20(0):3-37 [4135841.001]
  • [Cites] Brain Res. 1997 May 9;756(1-2):205-14 [9187334.001]
  • [Cites] Am J Clin Pathol. 1981 Mar;75(3):283-90 [7010989.001]
  • [Cites] Dev Biol. 1981 Jul 30;85(2):446-62 [7196351.001]
  • [Cites] Virchows Arch A Pathol Anat Histol. 1981;393(1):9-26 [6181610.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Feb;78(2):972-5 [16592982.001]
  • [Cites] Eur J Surg Oncol. 1995 Aug;21(4):388-90 [7664904.001]
  • [Cites] Am J Surg. 1995 Jun;169(6):595-9 [7771623.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10836-40 [8248178.001]
  • [Cites] FEMS Microbiol Lett. 2000 Oct 15;191(2):235-41 [11024269.001]
  • [Cites] J Pharmacol Exp Ther. 1998 May;285(2):619-27 [9580606.001]
  • [Cites] Bull World Health Organ. 1961;25:173-83 [13900274.001]
  • [Cites] Biochim Biophys Acta. 1969 May;181(1):93-104 [5792602.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Aug;78(8):4694-8 [6170978.001]
  • [Cites] J Neurochem. 1995 Dec;65(6):2585-93 [7595555.001]
  • [Cites] J Theor Biol. 1969 Oct;25(1):1-47 [4390734.001]
  • [Cites] Nouv Presse Med. 1973 Sep 8;2(31):2057 [4354299.001]
  • [Cites] Int J Gynecol Pathol. 1983;2(3):275-85 [6196309.001]
  • [Cites] J Cell Biol. 1980 Dec;87(3 Pt 1):611-28 [7462318.001]
  • [Cites] Science. 1990 Oct 12;250(4978):279-82 [2218531.001]
  • [Cites] J Biol Chem. 1993 Feb 15;268(5):3072-83 [8428986.001]
  • [Cites] Eur J Biochem. 1996 Apr 1;237(1):6-15 [8620894.001]
  • [Cites] J Exp Med. 1965 Mar 1;121:439-62 [14270243.001]
  • [Cites] Adv Cancer Res. 1979;29:275-346 [89800.001]
  • [Cites] Bacteriol Rev. 1964 Mar;28:2-13 [14127971.001]
  • [Cites] J Neurochem. 2000 Jun;74(6):2331-42 [10820193.001]
  • [Cites] Annu Rev Genet. 1971;5:407-24 [16097661.001]
  • [Cites] Biochemistry. 2001 Jul 10;40(27):8073-84 [11434776.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98 (11):6336-41 [11371646.001]
  • [Cites] J Theor Biol. 1976 May 21;58(2):455-76 [940335.001]
  • [Cites] Biochemistry. 1963 May-Jun;2:416-21 [14069522.001]
  • [Cites] Nat Neurosci. 2000 May;3(5):460-4 [10769385.001]
  • [Cites] Folia Microbiol (Praha). 1977;22(2):92-7 [191337.001]
  • [Cites] Biochem Biophys Res Commun. 2001 May 4;283(2):460-8 [11327724.001]
  • [Cites] Exp Neurol. 1995 Feb;131(2):193-202 [7895820.001]
  • [Cites] Free Radic Biol Med. 2001 Feb 15;30(4):447-50 [11182300.001]
  • [Cites] Anat Rec. 1981 Oct;201(2):203-23 [7032362.001]
  • [Cites] Zentralbl Bakteriol A. 1981 Aug;249(3):310-22 [7269855.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9328-32 [7568127.001]
  • [Cites] J Theor Biol. 1983 Jan 7;100(1):57-79 [6834861.001]
  • [Cites] Anticancer Res. 1997 Mar-Apr;17(2B):1379-82 [9137502.001]
  • [Cites] J Neurosci. 2001 Dec 1;21(23):9235-45 [11717357.001]
  • [Cites] Cancer Invest. 1995;13(2):227-38 [7874576.001]
  • [Cites] J Math Biol. 1982;14(2):133-51 [7119578.001]
  • [Cites] Annu Rev Biochem. 1985;54:73-100 [3927821.001]
  • [Cites] J Biol Chem. 1963 Jan;238:251-6 [13931033.001]
  • [Cites] J Theor Biol. 1969 Oct;25(1):49-107 [4390735.001]
  • [Cites] J Clin Invest. 1967 Jun;46(6):1010-6 [6067376.001]
  • [Cites] Folia Microbiol (Praha). 1980;25(1):40-9 [6243600.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4772-7 [9114067.001]
  • [Cites] Folia Microbiol (Praha). 2001;46(1):3-10 [11501471.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7951-5 [8367446.001]
  • [Cites] IUBMB Life. 2000 Apr;49(4):255-7 [10995025.001]
  • (PMID = 15954535.001).
  • [ISSN] 0015-5632
  • [Journal-full-title] Folia microbiologica
  • [ISO-abbreviation] Folia Microbiol. (Praha)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Bacterial Proteins; 0 / Biomarkers, Tumor; 0 / Intracellular Signaling Peptides and Proteins; 0 / Peptides; 0 / humanin; EC 3.2.2.5 / NAD+ Nucleosidase
  •  go-up   go-down


53. Burns DM, Li YL, Shi E, He C, Xu M, Zhuo J, Zhang C, Qian DQ, Li Y, Wynn R, Covington MB, Katiyar K, Marando CA, Fridman JS, Scherle P, Friedman S, Metcalf B, Yao W: Compelling P1 substituent affect on metalloprotease binding profile enables the design of a novel cyclohexyl core scaffold with excellent MMP selectivity and HER-2 sheddase inhibition. Bioorg Med Chem Lett; 2009 Jul 1;19(13):3525-30
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.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Antineoplastic Agents / chemical synthesis. Hydroxamic Acids / chemical synthesis. Membrane Proteins / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Drug Design. Humans. Matrix Metalloproteinase 2 / metabolism. Protein Binding. Structure-Activity Relationship. Substrate Specificity

  • BindingDB. BindingDB .
  • 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 = 19457660.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxamic Acids; 0 / Membrane Proteins; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.81 / ADAM10 protein, human
  •  go-up   go-down


54. Zhang D, Hanson R, Roongta V, Dischino DD, Gao Q, Sloan CP, Polson C, Keavy D, Zheng M, Mitroka J, Yeola S: In vitro and in vivo metabolism of a gamma-secretase inhibitor BMS-299897 and generation of active metabolites in milligram quantities with a microbial bioreactor. Curr Drug Metab; 2006 Dec;7(8):883-96
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.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Butyrates / metabolism. Cunninghamella / metabolism. Enzyme Inhibitors / metabolism. Hydrocarbons, Halogenated / metabolism
  • [MeSH-minor] Animals. Bile / metabolism. Bioreactors. Biotransformation. Carbon Radioisotopes. Cell Line, Tumor. Cells, Cultured. Dogs. Drug Evaluation, Preclinical. Glucuronides / metabolism. Hepatocytes / metabolism. Humans. Macaca fascicularis. Male. Microsomes, Liver / metabolism. Rats. Rats, Sprague-Dawley

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17168689.001).
  • [ISSN] 1389-2002
  • [Journal-full-title] Current drug metabolism
  • [ISO-abbreviation] Curr. Drug Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 4-(2-((1R)-1-(((4-chlorophenyl)sulfonyl)-2,5-difluoroanilino)ethyl)-5-fluorophenyl)butanoic acid; 0 / Butyrates; 0 / Carbon Radioisotopes; 0 / Enzyme Inhibitors; 0 / Glucuronides; 0 / Hydrocarbons, Halogenated; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


55. Qin B, Cartier L, Dubois-Dauphin M, Li B, Serrander L, Krause KH: A key role for the microglial NADPH oxidase in APP-dependent killing of neurons. Neurobiol Aging; 2006 Nov;27(11):1577-87
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.
  • Reactive oxygen species (ROS) and deposition of cleaved products of amyloid precursor protein (APP) are thought to contribute to neuronal loss observed in Alzheimer's disease (AD).

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16260066.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG019519; United States / NIAID NIH HHS / AI / R01 AI020866; United States / NIA NIH HHS / AG / AG19519-01; United States / NIAID NIH HHS / AI / AI20866-18
  • [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 / APP protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Antioxidants; 0 / Enzyme Inhibitors; 0 / Onium Compounds; 0 / Protease Nexins; 0 / Reactive Oxygen Species; 0 / Receptors, Cell Surface; 1406-18-4 / Vitamin E; 6HJ411TU98 / diphenyleneiodonium; EC 1.6.3.1 / NADPH Oxidase; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


56. Pinweha S, Wanikiat P, Sanvarinda Y, Supavilai P: The signaling cascades of Ganoderma lucidum extracts in stimulating non-amyloidogenic protein secretion in human neuroblastoma SH-SY5Y cell lines. Neurosci Lett; 2008 Dec 19;448(1):62-6
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.
  • In this study, we have investigated the effect of GL mycelia extracts on the non-amyloidogenic protein secretion (sAPPalpha) and the amyloid precursor protein (APP) expression in SH-SY5Y neuroblastoma cells.
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Amyloid beta-Protein Precursor / metabolism. Complex Mixtures / pharmacology. Reishi / chemistry. Signal Transduction / drug effects
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Neuroblastoma / metabolism. Protein Kinase C / metabolism

  • Genetic Alliance. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18938219.001).
  • [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] 0 / Amyloid beta-Protein Precursor; 0 / Complex Mixtures; 0 / Enzyme Inhibitors; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


57. Taddei K, Laws SM, Verdile G, Munns S, D'Costa K, Harvey AR, Martins IJ, Hill F, Levy E, Shaw JE, Martins RN: Novel phage peptides attenuate beta amyloid-42 catalysed hydrogen peroxide production and associated neurotoxicity. Neurobiol Aging; 2010 Feb;31(2):203-14
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] Novel phage peptides attenuate beta amyloid-42 catalysed hydrogen peroxide production and associated neurotoxicity.
  • Amyloid-beta (Abeta) peptides play a central role in the pathogenesis of Alzheimer's disease.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Bacteriophages / metabolism. Hydrogen Peroxide / metabolism. Neurons / physiology. Peptide Fragments / metabolism. Peptides / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Clioquinol / pharmacology. Escherichia coli / virology. Genetic Techniques. Humans. Hydro-Lyases / metabolism. Neuroprotective Agents / pharmacology. Peptide Library. Protein Binding. Rats. Sequence Analysis, DNA. Superoxide Dismutase / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CLIOQUINOL .
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18472186.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Neuroprotective Agents; 0 / Peptide Fragments; 0 / Peptide Library; 0 / Peptides; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 7BHQ856EJ5 / Clioquinol; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase; EC 4.2.1.- / Hydro-Lyases; EC 4.2.1.54 / lactate dehydratase
  •  go-up   go-down


58. Visser K, Smith C, Louw A: Interplay of the inflammatory and stress systems in a hepatic cell line: interactions between glucocorticoid receptor agonists and interleukin-6. Endocrinology; 2010 Nov;151(11):5279-93
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.
  • Like Dex, both CpdA and IL-6 increase the positive APPs, serum amyloid A and C-reactive protein, and decrease the negative APP, corticosteroid binding globulin.
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Western. Cell Line, Tumor. Cells, Cultured. Dexamethasone / pharmacology. Enzyme-Linked Immunosorbent Assay. Glucocorticoids / pharmacology. Mice. Reverse Transcriptase Polymerase Chain Reaction

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • 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 = 20881254.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Interleukin-6; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone
  •  go-up   go-down


59. Schwarz N, Pruessmeyer J, Hess FM, Dreymueller D, Pantaler E, Koelsch A, Windoffer R, Voss M, Sarabi A, Weber C, Sechi AS, Uhlig S, Ludwig A: Requirements for leukocyte transmigration via the transmembrane chemokine CX3CL1. Cell Mol Life Sci; 2010 Dec;67(24):4233-48
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.
  • [MeSH-minor] ADAM Proteins / genetics. ADAM Proteins / metabolism. ADAM10 Protein. ADAM17 Protein. Amino Acid Sequence. Amyloid Precursor Protein Secretases / genetics. Amyloid Precursor Protein Secretases / metabolism. Animals. Calcium Signaling / physiology. Cell Line, Tumor. Cells, Cultured. Chemotaxis / physiology. Endothelial Cells / cytology. Endothelial Cells / physiology. Epithelial Cells / cytology. Epithelial Cells / physiology. Humans. Ligands. Membrane Proteins / genetics. Membrane Proteins / metabolism. Molecular Sequence Data. Protein Structure, Secondary. Receptors, Chemokine / chemistry. Receptors, Chemokine / genetics. Receptors, Chemokine / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Aug 15;102(4):1186-95 [12714508.001]
  • [Cites] J Immunol. 2007 Jun 15;178(12 ):8064-72 [17548644.001]
  • [Cites] J Leukoc Biol. 2003 Jan;73(1):30-48 [12525560.001]
  • [Cites] Eur J Immunol. 2003 Mar;33(3):729-39 [12616493.001]
  • [Cites] Cell. 1997 Nov 14;91(4):521-30 [9390561.001]
  • [Cites] J Clin Invest. 2003 Apr;111(8):1241-50 [12697743.001]
  • [Cites] Thromb Haemost. 2007 May;97(5):694-703 [17479179.001]
  • [Cites] Blood. 2000 May 15;95(10):3032-43 [10807766.001]
  • [Cites] J Biol Chem. 1994 Aug 26;269(34):21755-61 [8063819.001]
  • [Cites] Science. 2005 Jan 14;307(5707):254-8 [15653504.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34183-9 [10940307.001]
  • [Cites] Nature. 1997 Feb 13;385(6617):640-4 [9024663.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4588-97 [9373270.001]
  • [Cites] J Biol Chem. 2007 Feb 23;282(8):5111-5 [17197449.001]
  • [Cites] Annu Rev Immunol. 2004;22:891-928 [15032599.001]
  • [Cites] J Clin Invest. 2003 Feb;111(3):333-40 [12569158.001]
  • [Cites] J Biol Chem. 2001 Oct 12;276(41):37993-8001 [11495925.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1999 Nov-Dec;35(10):558-9 [10614862.001]
  • [Cites] J Immunol. 2002 Jan 15;168(2):604-12 [11777952.001]
  • [Cites] J Biol Chem. 1998 Sep 11;273(37):23799-804 [9726990.001]
  • [Cites] Biochim Biophys Acta. 2007 Apr;1768(4):913-22 [17084806.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34408-18 [11448957.001]
  • [Cites] Mol Pharmacol. 2005 Jun;67(6):1966-76 [15761117.001]
  • [Cites] J Biol Chem. 1994 Jan 28;269(4):2790-5 [7507928.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10896-901 [9724801.001]
  • [Cites] J Biol Chem. 2010 Jan 1;285(1):555-64 [19875451.001]
  • [Cites] Blood. 2003 Jan 15;101(2):399-406 [12393663.001]
  • [Cites] Circulation. 2003 Feb 25;107(7):1009-16 [12600915.001]
  • [Cites] J Exp Med. 1998 Oct 19;188(8):1413-9 [9782118.001]
  • [Cites] J Biol Chem. 1995 Apr 21;270(16):9121-8 [7721826.001]
  • [Cites] Comb Chem High Throughput Screen. 2005 Mar;8(2):161-71 [15777180.001]
  • [Cites] Biochem Biophys Res Commun. 2010 Apr 30;395(2):178-84 [20347720.001]
  • [Cites] Cell. 1994 Jan 28;76(2):301-14 [7507411.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 21;101(51):17795-800 [15596719.001]
  • [Cites] Semin Cell Dev Biol. 2009 Apr;20(2):164-74 [18951988.001]
  • [Cites] J Biol Chem. 1999 Apr 9;274(15):10053-8 [10187784.001]
  • (PMID = 20559678.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CX3CL1 protein, human; 0 / CX3CR1 protein, human; 0 / Chemokine CX3CL1; 0 / Ligands; 0 / Membrane Proteins; 0 / Receptors, Chemokine; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 Protein; EC 3.4.24.81 / ADAM10 protein, human; EC 3.4.24.86 / ADAM17 Protein
  •  go-up   go-down


60. Yanagida K, Okochi M, Tagami S, Nakayama T, Kodama TS, Nishitomi K, Jiang J, Mori K, Tatsumi S, Arai T, Ikeuchi T, Kasuga K, Tokuda T, Kondo M, Ikeda M, Deguchi K, Kazui H, Tanaka T, Morihara T, Hashimoto R, Kudo T, Steiner H, Haass C, Tsuchiya K, Akiyama H, Kuwano R, Takeda M: The 28-amino acid form of an APLP1-derived Abeta-like peptide is a surrogate marker for Abeta42 production in the central nervous system. EMBO Mol Med; 2009 Jul;1(4):223-35
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.
  • Surrogate markers for the Alzheimer disease (AD)-associated 42-amino acid form of amyloid-beta (Abeta42) have been sought because they may aid in the diagnosis of AD and for clarification of disease pathogenesis.
  • [MeSH-major] Alzheimer Disease / diagnosis. Amyloid beta-Protein Precursor / cerebrospinal fluid. Biomarkers / cerebrospinal fluid. Peptide Fragments / cerebrospinal fluid
  • [MeSH-minor] Adult. Amino Acid Sequence. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Aspartic Acid Endopeptidases / antagonists & inhibitors. Aspartic Acid Endopeptidases / metabolism. Cell Line. Cell Line, Tumor. Humans. Middle Aged. Molecular Sequence Data. Mutation. Presenilin-1 / genetics

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1999 Oct 22;286(5440):735-41 [10531052.001]
  • [Cites] Nat Med. 2005 May;11(5):545-50 [15834426.001]
  • [Cites] Nature. 1999 Dec 2;402(6761):533-7 [10591213.001]
  • [Cites] Nature. 1999 Dec 2;402(6761):537-40 [10591214.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):390-7 [10617630.001]
  • [Cites] Arch Neurol. 2000 Jan;57(1):100-5 [10634455.001]
  • [Cites] Mol Cell Neurosci. 1999 Dec;14(6):419-27 [10656250.001]
  • [Cites] Neurochem Int. 2000 Mar;36(3):175-84 [10676850.001]
  • [Cites] Eur Neurol. 2000;43(3):155-60 [10765056.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9712-7 [10931940.001]
  • [Cites] Nature. 2000 Sep 7;407(6800):48-54 [10993067.001]
  • [Cites] Mol Cell Neurosci. 2000 Nov;16(5):609-19 [11083922.001]
  • [Cites] J Biol Chem. 2000 Dec 29;275(52):40925-32 [11013240.001]
  • [Cites] Physiol Rev. 2001 Apr;81(2):741-66 [11274343.001]
  • [Cites] Nature. 2001 Nov 8;414(6860):212-6 [11700559.001]
  • [Cites] Dev Cell. 2002 Jul;3(1):85-97 [12110170.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5408-16 [12374741.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):44754-9 [12223485.001]
  • [Cites] Nature. 2003 Mar 27;422(6930):438-41 [12660785.001]
  • [Cites] Neuron. 2003 Apr 10;38(1):9-12 [12691659.001]
  • [Cites] Nat Cell Biol. 2003 May;5(5):486-8 [12679784.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6382-7 [12740439.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18146-56 [14970212.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):24343-54 [15037614.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4245-9 [3159021.001]
  • [Cites] Ann Neurol. 1995 Oct;38(4):643-8 [7574461.001]
  • [Cites] J Neurochem. 1996 Jan;66(1):259-65 [8522962.001]
  • [Cites] J Biol Chem. 2005 Jun 17;280(24):23009-17 [15824102.001]
  • [Cites] Neurosci Res. 2006 Apr;54(4):235-53 [16457902.001]
  • [Cites] J Biol Chem. 2006 Mar 24;281(12):7890-8 [16434391.001]
  • [Cites] J Biol Chem. 2007 Apr 20;282(16):11982-95 [17307738.001]
  • [Cites] J Neurochem. 2007 May;101(4):1053-9 [17254013.001]
  • [Cites] Ann Neurol. 2007 May;61(5):446-53 [17366635.001]
  • [Cites] Nature. 2008 Jun 12;453(7197):925-9 [18548070.001]
  • [Cites] J Biol Chem. 1996 Sep 13;271(37):22908-14 [8798471.001]
  • [Cites] Neuron. 1996 Nov;17(5):1005-13 [8938131.001]
  • [Cites] Nat Med. 1997 Jan;3(1):67-72 [8986743.001]
  • [Cites] FEBS Lett. 1997 Nov 24;418(1-2):162-6 [9414118.001]
  • [Cites] Ann Neurol. 1999 Apr;45(4):504-11 [10211475.001]
  • [Cites] Arch Neurol. 1999 Jun;56(6):673-80 [10369305.001]
  • [Cites] J Neurosci. 1999 Oct 15;19(20):8876-84 [10516307.001]
  • [CommentIn] EMBO Mol Med. 2009 Jul;1(4):195-7 [20049720.001]
  • (PMID = 20049724.001).
  • [ISSN] 1757-4684
  • [Journal-full-title] EMBO molecular medicine
  • [ISO-abbreviation] EMBO Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APLP1 protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Biomarkers; 0 / PSEN1 protein, human; 0 / Peptide Fragments; 0 / Presenilin-1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  • [Other-IDs] NLM/ PMC3378133
  •  go-up   go-down


61. Tamura Y, Hamajima K, Matsui K, Yanoma S, Narita M, Tajima N, Xin KQ, Klinman D, Okuda K: The F(ab)'2 fragment of an Abeta-specific monoclonal antibody reduces Abeta deposits in the brain. Neurobiol Dis; 2005 Nov;20(2):541-9
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.
  • This work examines whether administering the F(ab' )2 fragment of an IgG1 monoclonal antibody (mAb) targeting the N-terminal 1-13 amino acids of the beta-amyloid peptide (Abeta mAb) reduces amyloid deposition in Alzheimer's disease (AD).
  • Since IgG1 Abs do not fix complement, these findings suggest that effective in vivo clearance of amyloid deposits can be achieved without stimulation of FcR-reactive phagocytes or activation of the complement cascade.
  • [MeSH-major] Alzheimer Disease / drug therapy. Amyloid beta-Peptides / antagonists & inhibitors. Antibodies, Monoclonal / pharmacology. Immunoglobulin Fab Fragments / pharmacology. Plaque, Amyloid / drug effects
  • [MeSH-minor] Animals. Brain / drug effects. Brain / immunology. Brain / physiopathology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Complement System Proteins / drug effects. Complement System Proteins / immunology. Complement System Proteins / metabolism. Disease Models, Animal. Encephalitis / drug therapy. Encephalitis / immunology. Encephalitis / prevention & control. Injections, Intraperitoneal. Injections, Intraventricular. Mice. Mice, Transgenic. Peptide Fragments / antagonists & inhibitors. Peptide Fragments / chemistry. Peptide Fragments / immunology. Phagocytes / drug effects. Phagocytes / physiology. Protein Structure, Tertiary / drug effects. Protein Structure, Tertiary / physiology

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15908227.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fab Fragments; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 9007-36-7 / Complement System Proteins
  •  go-up   go-down


62. Wasilewska-Sampaio AP, Silveira MS, Holub O, Goecking R, Gomes FC, Neto VM, Linden R, Ferreira ST, De Felice FG: Neuritogenesis and neuronal differentiation promoted by 2,4-dinitrophenol, a novel anti-amyloidogenic compound. FASEB J; 2005 Oct;19(12):1627-36
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.
  • We examined the effects of 2,4-dinitrophenol (DNP), a recently described blocker of the aggregation and neurotoxicity of the beta-amyloid peptide, on neurite elongation of central neurons.
  • [MeSH-major] 2,4-Dinitrophenol / pharmacology. Amyloid / chemistry. Neurites / pathology. Neurons / metabolism
  • [MeSH-minor] Amyloid beta-Peptides / chemistry. Animals. Blotting, Western. Cell Differentiation. Cell Line. Cell Line, Tumor. Cerebral Cortex / pathology. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Extracellular Signal-Regulated MAP Kinases / metabolism. Hippocampus / cytology. Hippocampus / embryology. MAP Kinase Signaling System. Mice. Microscopy, Fluorescence. Neurodegenerative Diseases / pathology. Oxygen / metabolism. Oxygen Consumption. Peptide Fragments / chemistry. Rats. Reactive Oxygen Species. Time Factors. Uncoupling Agents / pharmacology. tau Proteins / chemistry

  • Hazardous Substances Data Bank. 2,4-Dinitrophenol .
  • Hazardous Substances Data Bank. OXYGEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16195371.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / Reactive Oxygen Species; 0 / Uncoupling Agents; 0 / tau Proteins; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; Q13SKS21MN / 2,4-Dinitrophenol; S88TT14065 / Oxygen
  •  go-up   go-down


63. Wang Q, Li H, Liu N, Chen XY, Wu ML, Zhang KL, Kong QY, Liu J: Correlative analyses of notch signaling with resveratrol-induced differentiation and apoptosis of human medulloblastoma cells. Neurosci Lett; 2008 Jun 20;438(2):168-73
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.
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Active Transport, Cell Nucleus / physiology. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Antioxidants / pharmacology. Antioxidants / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. Basic Helix-Loop-Helix Transcription Factors / drug effects. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cytoplasm / drug effects. Cytoplasm / metabolism. Enzyme Inhibitors / pharmacology. Homeodomain Proteins / drug effects. Homeodomain Proteins / metabolism. Humans. Receptor, Notch1 / drug effects. Receptor, Notch1 / metabolism. Receptor, Notch2 / drug effects. Receptor, Notch2 / metabolism. Up-Regulation / drug effects. Up-Regulation / physiology

  • Genetic Alliance. consumer health - Medulloblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • Hazardous Substances Data Bank. RESVERATROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18456406.001).
  • [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] 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; 0 / Receptors, Notch; 0 / Stilbenes; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases; Q369O8926L / resveratrol
  •  go-up   go-down


64. Li YB, Wang R, Wu HL, Li YH, Zhong LJ, Yu HM, Li XJ: Serum amyloid A mediates the inhibitory effect of Ganoderma lucidum polysaccharides on tumor cell adhesion to endothelial cells. Oncol Rep; 2008 Sep;20(3):549-56
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] Serum amyloid A mediates the inhibitory effect of Ganoderma lucidum polysaccharides on tumor cell adhesion to endothelial cells.
  • The present study was designed to determine the anti-tumor efficacy of GlPS and the possible mechanism covering this effect.
  • Three significantly changed proteins were identified by ESI-Q-TOF-MS and database search indicated that they were haptoblobin, apolipoprotein A-II and serum amyloid A (SAA), respectively.
  • Collectively, these results suggest that GlPS inhibited the tumor growth and tumor cell adhesion to HUVECs via up-regulation of SAA protein expression.
  • [MeSH-major] Cell Adhesion / drug effects. Endothelium, Vascular / metabolism. Polysaccharides / therapeutic use. Prostatic Neoplasms / metabolism. Reishi / chemistry. Sarcoma 180 / drug therapy. Serum Amyloid A Protein / metabolism

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18695905.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Polysaccharides; 0 / RNA, Messenger; 0 / Serum Amyloid A Protein
  •  go-up   go-down


65. Serdar A, Basak D, Sercan G, Ali V: Solitary amyloid tumor of the tongue base. Int J Otolaryngol; 2009;2009:515068
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] Solitary amyloid tumor of the tongue base.
  • The purpose of this article is to present a rare case of localized, solitary amyloid tumor of tongue base and emphasize some of the characteristic features of challenging clinical and histopathologic diagnosis.
  • In this paper, we focused on the clinical and pathological specifications of this rare tumor, so any unnecessary examinations or measures may be spared.
  • Negative staining of amyloid material with AAC and osseous metaplasia noted in the histopathologic examination may not be thought as definite criteria for localized amyloidosis, but a supporter of localized, solitary amyloid tumor diagnosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Diagn Cytopathol. 2001 Mar;24(3):181-5 [11241901.001]
  • [Cites] Oral Oncol. 2006 Apr;42(4):421-9 [16488655.001]
  • [Cites] Am J Otolaryngol. 2004 May-Jun;25(3):186-9 [15124168.001]
  • [Cites] Diagn Cytopathol. 1993 Oct;9(5):570-5 [8287770.001]
  • (PMID = 20107570.001).
  • [ISSN] 1687-921X
  • [Journal-full-title] International journal of otolaryngology
  • [ISO-abbreviation] Int J Otolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2809435
  •  go-up   go-down


66. von Arnim CA, von Einem B, Weber P, Wagner M, Schwanzar D, Spoelgen R, Strauss WL, Schneckenburger H: Impact of cholesterol level upon APP and BACE proximity and APP cleavage. Biochem Biophys Res Commun; 2008 May 30;370(2):207-12
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.
  • Cleavage of APP by BACE is the first proteolytic step in the production of Amyloid beta (Abeta, which accumulates in senile plaques in Alzheimer's disease.
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Amyloid beta-Protein Precursor / metabolism. Aspartic Acid Endopeptidases / metabolism. Cell Membrane / metabolism. Cholesterol / metabolism. Fluorescence Resonance Energy Transfer / methods. Microscopy, Fluorescence / methods. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Cell Line, Tumor. Green Fluorescent Proteins / analysis. Green Fluorescent Proteins / genetics. Humans. Membrane Fluidity. Protease Nexins

  • MedlinePlus Health Information. consumer health - Cholesterol.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18374657.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APP protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Protease Nexins; 0 / Receptors, Cell Surface; 147336-22-9 / Green Fluorescent Proteins; 97C5T2UQ7J / Cholesterol; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  •  go-up   go-down


67. Elzinga BM, Twomey C, Powell JC, Harte F, McCarthy JV: Interleukin-1 receptor type 1 is a substrate for gamma-secretase-dependent regulated intramembrane proteolysis. J Biol Chem; 2009 Jan 16;284(3):1394-409
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 this study, we report the characterization of a highly conserved tumor necrosis factor receptor-associated factor-6 (TRAF6) consensus-binding site within the hydrophilic loop domain of presenilin-1 (PS-1).
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Interleukin-1 Receptor-Associated Kinases / metabolism. Presenilin-1 / metabolism. Receptors, Interleukin-1 Type I / metabolism. TNF Receptor-Associated Factor 6 / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18996842.001).
  • [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 / Cytokines; 0 / IL1R1 protein, human; 0 / Presenilin-1; 0 / Protease Inhibitors; 0 / Receptors, Interleukin-1 Type I; 0 / TNF Receptor-Associated Factor 6; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


68. Tang H, Fu Y, Cui Y, He Y, Zeng X, Ploplis VA, Castellino FJ, Luo Y: Fibrinogen has chaperone-like activity. Biochem Biophys Res Commun; 2009 Jan 16;378(3):662-7
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] Fibrinogen has chaperone-like activity.
  • Partially or completely unfolded polypeptides are highly prone to aggregation due to nonspecific interactions between their exposed hydrophobic surfaces.
  • Extracellular proteins are continuously subjected to stresses conditions, but the existence of extracellular chaperones remains largely unexplored.
  • The results presented here demonstrate that one of the most abundant extracellular proteins, fibrinogen has chaperone-like activity.
  • Fibrinogen can specifically bind to nonnative form of citrate synthase and inhibit its thermal aggregation and inactivation in an ATP-independent manner.
  • Interestingly, fibrinogen maintains thermal-denatured luciferase in a refolding competent state allowing luciferase to be refolded in cooperation with rabbit reticulocyte lysate.
  • Fibrinogen also inhibits fibril formation of yeast prion protein Sup35 (NM).
  • Furthermore, fibrinogen rescues thermal-induced protein aggregation in the plasma of fibrinogen-deficient mice.
  • Our studies demonstrate the chaperone-like activity of fibrinogen, which not only provides new insights into the extracellular chaperone protein system, but also suggests potential diagnostic and therapeutic approaches to fibrinogen-related pathological conditions.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEBS Lett. 2000 May 12;473(2):199-202 [10812074.001]
  • [Cites] Diabet Med. 2007 Oct;24(10):1143-8 [17888134.001]
  • [Cites] Am J Pathol. 2000 Sep;157(3):703-8 [10980108.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Sep;85(9):3121-5 [10999796.001]
  • [Cites] Nature. 2000 Nov 23;408(6811):479-83 [11100730.001]
  • [Cites] Annu Rev Biochem. 2001;70:603-47 [11395418.001]
  • [Cites] Nature. 2002 Apr 4;416(6880):507-11 [11932737.001]
  • [Cites] Trends Mol Med. 2002 Aug;8(8):370-4 [12127722.001]
  • [Cites] J Clin Invest. 2002 Nov;110(9):1221-32 [12417558.001]
  • [Cites] Curr Biol. 2002 Oct 29;12(21):1833-9 [12419183.001]
  • [Cites] Nature. 2003 Aug 21;424(6951):948-51 [12931190.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):3-16 [15036202.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):17-29 [15036203.001]
  • [Cites] Lancet. 2004 Apr 3;363(9415):1139-46 [15064035.001]
  • [Cites] J Biol Chem. 1983 Apr 10;258(7):4249-56 [6833255.001]
  • [Cites] N Engl J Med. 1984 Aug 23;311(8):501-5 [6749207.001]
  • [Cites] Annu Rev Biochem. 1984;53:195-229 [6383194.001]
  • [Cites] Nat Genet. 1993 Mar;3(3):252-5 [8097946.001]
  • [Cites] J Clin Invest. 1994 Feb;93(2):731-6 [8113408.001]
  • [Cites] Nature. 1994 Jul 14;370(6485):111-7 [8022479.001]
  • [Cites] Blood. 1996 May 15;87(10):4197-203 [8639778.001]
  • [Cites] Nature. 1996 Jun 13;381(6583):571-9 [8637592.001]
  • [Cites] J Cardiovasc Risk. 1996 Jun;3(3):307-11 [8863104.001]
  • [Cites] EMBO J. 1997 Feb 3;16(3):659-71 [9034347.001]
  • [Cites] Nature. 1997 Feb 27;385(6619):787-93 [9039909.001]
  • [Cites] Cell. 1997 May 30;89(5):811-9 [9182769.001]
  • [Cites] Methods Enzymol. 1998;290:323-38 [9534173.001]
  • [Cites] Cell. 1998 Jul 10;94(1):73-82 [9674429.001]
  • [Cites] Clin Immunol. 1999 Jan;90(1):89-99 [9884356.001]
  • [Cites] N Engl J Med. 1999 Feb 11;340(6):448-54 [9971870.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):6875-81 [10066740.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Jul;31(7):741-6 [10467729.001]
  • [Cites] Trends Biochem Sci. 1999 Sep;24(9):329-32 [10470028.001]
  • [Cites] Stroke. 2005 Dec;36(12):2637-41 [16269641.001]
  • [Cites] EMBO Rep. 2005 Dec;6(12):1131-6 [16319958.001]
  • [Cites] Blood. 2006 May 15;107(10):3883-91 [16434491.001]
  • [Cites] Cell. 2006 May 5;125(3):443-51 [16678092.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6412-7 [17404210.001]
  • [Cites] J Mol Biol. 2007 May 25;369(1):157-67 [17407782.001]
  • [Cites] Trends Biochem Sci. 2007 May;32(5):217-24 [17412596.001]
  • [Cites] N Engl J Med. 2000 Aug 10;343(6):411-9 [10933741.001]
  • (PMID = 19059206.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL073750-01A19002; United States / NHLBI NIH HHS / HL / P01 HL073750; United States / NHLBI NIH HHS / HL / HL073750; United States / NHLBI NIH HHS / HL / P01 HL073750-01A19002
  • [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 / Amyloid; 0 / Molecular Chaperones; 0 / Peptide Termination Factors; 0 / Prions; 0 / SUP35 protein, S cerevisiae; 0 / Saccharomyces cerevisiae Proteins; 9001-32-5 / Fibrinogen; EC 1.13.12.7 / Luciferases, Firefly; EC 2.3.3.1 / Citrate (si)-Synthase
  • [Other-IDs] NLM/ NIHMS92328; NLM/ PMC2663026
  •  go-up   go-down


69. Madeira A, Pommet JM, Prochiantz A, Allinquant B: SET protein (TAF1beta, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain. FASEB J; 2005 Nov;19(13):1905-7
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] SET protein (TAF1beta, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain.
  • When overexpressed, a short cytoplasmic domain of the amyloid precursor protein (APP), normally unmasked in the brain of Alzheimer's disease patients, activates caspase-3 and induces neuronal death.
  • [MeSH-major] Amyloid beta-Protein Precursor / chemistry. Apoptosis. Chromosomal Proteins, Non-Histone / physiology. Cytoplasm / metabolism. Neurons / pathology. Transcription Factors / physiology
  • [MeSH-minor] Alzheimer Disease / metabolism. Animals. Aspartic Acid / chemistry. Biological Assay. Brain / embryology. Cell Death. Cell Line, Tumor. Cell Survival. Down-Regulation. Histone Chaperones. Humans. Immunohistochemistry. Mass Spectrometry. Models, Biological. Oligonucleotides, Antisense / chemistry. Oligonucleotides, Antisense / pharmacology. Peptides / chemistry. Protein Binding. Protein Structure, Tertiary. Rats. Recombinant Proteins / chemistry. Silver Staining. Tyrosine / chemistry

  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. L-TYROSINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16162853.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Oligonucleotides, Antisense; 0 / Peptides; 0 / Recombinant Proteins; 0 / SET protein, human; 0 / Transcription Factors; 30KYC7MIAI / Aspartic Acid; 42HK56048U / Tyrosine
  •  go-up   go-down


70. Rallidis LS, Hamodraka ES, Fountoulaki K, Moustogiannis G, Zolindaki MG, Kremastinos DT: Simvastatin exerts its anti-inflammatory effect in hypercholesterolaemic patients by decreasing the serum levels of monocyte chemoattractant protein-1. Int J Cardiol; 2008 Feb 29;124(2):271-2
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.
  • AIM: To assess the effect of simvastatin on serum levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6, tumor necrosis factor-alpha, macrophage colony stimulating factor, C-reactive protein and serum amyloid A in hypercholesterolaemic patients without coronary heart disease.
  • [MeSH-minor] Adult. Aged. Amyloid / blood. Amyloid / drug effects. Biomarkers / blood. C-Reactive Protein / drug effects. C-Reactive Protein / metabolism. Cardiovascular Diseases / prevention & control. Cytokines / drug effects. Cytokines / metabolism. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Probability. Reference Values. Risk Factors. Sensitivity and Specificity. Severity of Illness Index. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cholesterol.
  • Hazardous Substances Data Bank. SIMVASTATIN .
  • 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 = 17399814.001).
  • [ISSN] 1874-1754
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Letter; Randomized Controlled Trial
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid; 0 / Biomarkers; 0 / Chemokine CCL2; 0 / Cytokines; 9007-41-4 / C-Reactive Protein; AGG2FN16EV / Simvastatin
  •  go-up   go-down


71. Wang R, Chadalavada K, Wilshire J, Kowalik U, Hovinga KE, Geber A, Fligelman B, Leversha M, Brennan C, Tabar V: Glioblastoma stem-like cells give rise to tumour endothelium. Nature; 2010 Dec 09;468(7325):829-33
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] Glioblastoma stem-like cells give rise to tumour endothelium.
  • Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined.
  • Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7.
  • Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell.
  • The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium.
  • Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors.
  • The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.
  • [MeSH-minor] AC133 Antigen. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Bevacizumab. Cadherins / deficiency. Cadherins / metabolism. Cell Line, Tumor. Cell Lineage. Chromosome Aberrations. Coculture Techniques. Female. Glycoproteins / metabolism. Humans. In Situ Hybridization, Fluorescence. Integrin beta4 / metabolism. Male. Mice. Mice, Inbred NOD. Mice, SCID. Peptides / metabolism. Receptor, Notch1 / deficiency. Receptor, Notch1 / genetics. Vascular Endothelial Growth Factor A / antagonists & inhibitors

  • Genetic Alliance. consumer health - Glioblastoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Nat Rev Cancer. 2011 Jan;11(1):4 [21218530.001]
  • [CommentIn] Nat Rev Neurosci. 2011 Jan;12(1):3 [21218567.001]
  • [CommentIn] Nature. 2010 Dec 9;468(7325):770-1 [21150987.001]
  • (PMID = 21102433.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE24244/ GSE24446/ GSE24452/ GSE24557/ GSE24558
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Cadherins; 0 / Glycoproteins; 0 / Integrin beta4; 0 / PROM1 protein, human; 0 / Peptides; 0 / Prom1 protein, mouse; 0 / Receptor, Notch1; 0 / Vascular Endothelial Growth Factor A; 0 / cadherin 5; 2S9ZZM9Q9V / Bevacizumab; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


72. Rasul S, Balasubramanian R, Filipović A, Slade MJ, Yagüe E, Coombes RC: Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells. Br J Cancer; 2009 Jun 16;100(12):1879-88
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] Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells.
  • Gamma-secretase activity is vital for the transmembrane cleavage of Notch receptors and the subsequent migration of their intracellular domains to the nucleus.
  • Notch overexpression has been associated with breast, colon, cervical and prostate cancers.
  • We tested the effect of three different gamma-secretase inhibitors (GSIs) in breast cancer cells.
  • One inhibitor (GSI1) was lethal to breast cancer cell lines at concentrations of 2 muM and above but had a minimal effect on the non-malignant breast lines.
  • GSI1 was also cytotoxic for a wide variety of cancer cell lines in the NCI60 cell screen.
  • GSI1 treatment resulted in a marked decrease in gamma-secretase activity and downregulation of the Notch signalling pathway with no effects on expression of the gamma-secretase components or ligands.
  • Flow cytometric and western blot analyses indicated that GSI1 induces a G2/M arrest leading to apoptosis, through downregulation of Bcl-2, Bax and Bcl-XL.
  • GSI1 also inhibited proteasome activity.
  • Thus, the gamma-secretase inhibitor GSI1 has a complex mode of action to inhibit breast cancer cell survival and may represent a novel therapy in breast cancer.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • 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] Clin Cancer Res. 2005 Aug 15;11(16):5833-9 [16115923.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2353-63 [15781650.001]
  • [Cites] Biochem J. 2005 Nov 1;391(Pt 3):513-25 [15975090.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1517-25 [16452208.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):6889-94 [16636269.001]
  • [Cites] Mol Pharm. 2006 Jan-Feb;3(1):33-44 [16686367.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9262-7 [16751266.001]
  • [Cites] J Biol Chem. 2006 Oct 27;281(43):32870-8 [16951406.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5652-7 [17116942.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):350-2 [16504380.001]
  • [Cites] Cancer Sci. 2007 Feb;98(2):155-62 [17297654.001]
  • [Cites] Lancet Oncol. 2007 Mar;8(3):235-44 [17329194.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1879-82 [17332312.001]
  • [Cites] Nat Protoc. 2006;1(3):1112-6 [17406391.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 18;99(8):616-27 [17440163.001]
  • [Cites] Mod Pathol. 2007 Jun;20(6):685-93 [17507991.001]
  • [Cites] Neoplasia. 2007 May;9(5):427-34 [17534448.001]
  • [Cites] Cell Biol Int. 2007 Oct;31(10):1136-43 [17493842.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8051-7 [17804716.001]
  • [Cites] Oral Dis. 2007 Nov;13(6):555-63 [17944672.001]
  • [Cites] Int J Gynecol Cancer. 2007 Nov-Dec;17(6):1293-9 [17388915.001]
  • [Cites] J Surg Oncol. 2008 Jan 1;97(1):63-8 [17918209.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):131-44 [18166351.001]
  • [Cites] Int J Cancer. 2008 Mar 1;122(5):1058-67 [17955490.001]
  • [Cites] Nature. 2008 Jan 3;451(7174):76-80 [18172499.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2220-9 [18039953.001]
  • [Cites] Cancer Res. 2008 Mar 15;68(6):1881-8 [18339869.001]
  • [Cites] Haematologica. 2008 Apr;93(4):533-42 [18322257.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):5226-35 [18593923.001]
  • [Cites] Oncogene. 2008 Aug 28;27(37):5019-32 [18469855.001]
  • [Cites] BMC Biochem. 2008;9 Suppl 1:S2 [19007432.001]
  • [Cites] Mol Cell Biol. 2004 Sep;24(17):7612-21 [15314169.001]
  • [Cites] Oncogene. 2000 Jan 13;19(2):223-31 [10645000.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(22):7761-74 [11604511.001]
  • [Cites] Science. 2001 Dec 7;294(5549):2179-81 [11679632.001]
  • [Cites] EMBO J. 2002 Apr 15;21(8):1948-56 [11953314.001]
  • [Cites] Nat Med. 2002 Sep;8(9):979-86 [12185362.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):44754-9 [12223485.001]
  • [Cites] J Cell Physiol. 2003 Mar;194(3):237-55 [12548545.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):827-36 [12576456.001]
  • [Cites] J Biol Chem. 2003 Jun 20;278(25):23196-203 [12682059.001]
  • [Cites] Clin Cancer Res. 2003 Dec 15;9(17):6316-25 [14695130.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3037-45 [15126339.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Jun;5(6):499-504 [15173829.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):171-83 [15324700.001]
  • [Cites] J Cell Biol. 2004 Oct 25;167(2):215-21 [15492044.001]
  • [Cites] Immunopharmacology. 1992 Jan-Feb;23(1):37-48 [1349009.001]
  • [Cites] Cell. 1995 Mar 24;80(6):909-17 [7697721.001]
  • [Cites] Mol Cell Biol. 1996 Mar;16(3):952-9 [8622698.001]
  • [Cites] Cancer Res. 1996 Apr 15;56(8):1775-85 [8620493.001]
  • [Cites] Curr Biol. 1995 Dec 1;5(12):1416-23 [8749394.001]
  • [Cites] Biochemistry. 1997 Dec 9;36(49):15396-403 [9398269.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8530-7 [16166334.001]
  • (PMID = 19513078.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Receptors, Notch; 0 / bcl-2-Associated X Protein; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2714234
  •  go-up   go-down


73. van der Hilst JC, Simon A, Drenth JP: Hereditary periodic fever and reactive amyloidosis. Clin Exp Med; 2005 Oct;5(3):87-98
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.
  • Familial Mediterranean fever (FMF) is the most frequent entity within this group of disorders which further consists of hyperimmunoglobulinaemia D and periodic fever syndrome (HIDS), tumour necrosis factor receptor-associated periodic syndrome (TRAPS) and cryopyrin-associated periodic syndrome (CAPS).
  • This is caused by deposition of fibrils that consist of the proteolytically cleaved acutephase protein serum amyloid A (SAA).
  • [MeSH-minor] Carrier Proteins / genetics. Humans. Hypergammaglobulinemia / genetics. Immunoglobulin D / genetics. Prognosis. Receptors, Tumor Necrosis Factor / genetics. Serum Amyloid A Protein / metabolism

  • Genetic Alliance. consumer health - Amyloidosis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16284730.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Immunoglobulin D; 0 / NLRP3 protein, human; 0 / Receptors, Tumor Necrosis Factor; 0 / Serum Amyloid A Protein
  • [Number-of-references] 167
  •  go-up   go-down


74. Bolognin S, Zatta P, Drago D, Tognon G, Parnigotto PP, Ricchelli F: Mutual stimulation of beta-amyloid fibrillogenesis by clioquinol and divalent metals. Neuromolecular Med; 2008;10(4):322-32
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] Mutual stimulation of beta-amyloid fibrillogenesis by clioquinol and divalent metals.
  • Its biological effects are most likely ascribed to complexation of specific metal ions, such as copper (II) and zinc (II), critically associated with beta-amyloid (A beta) aggregation/fibrillogenesis and degeneration processes in the brain.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid beta-Peptides / drug effects. Clioquinol / pharmacology. Metals / toxicity. Plaque, Amyloid / drug effects
  • [MeSH-minor] Amino Acid Substitution / drug effects. Amino Acid Substitution / physiology. Animals. Cell Line, Tumor. Chelation Therapy / adverse effects. Chelation Therapy / methods. Copper / toxicity. Drug Synergism. Humans. Neurotoxins / toxicity. Rats. Species Specificity. Zinc / toxicity

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • Hazardous Substances Data Bank. CLIOQUINOL .
  • Hazardous Substances Data Bank. COPPER, ELEMENTAL .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Neuromolecular Med. 2008;10(4):393
  • [Cites] Int J Exp Pathol. 2005 Jun;86(3):147-59 [15910549.001]
  • [Cites] Biochemistry. 2000 Jun 13;39(23):7024-31 [10841784.001]
  • [Cites] Biochemistry. 2006 May 30;45(21):6724-32 [16716083.001]
  • [Cites] Ann N Y Acad Sci. 2000;920:292-304 [11193167.001]
  • [Cites] J Neurochem. 1995 Jul;65(1):218-27 [7790863.001]
  • [Cites] Protein Sci. 1993 Mar;2(3):404-10 [8453378.001]
  • [Cites] Breast Cancer Res. 2005;7(6):R897-908 [16280039.001]
  • [Cites] Science. 1996 Oct 4;274(5284):99-102 [8810256.001]
  • [Cites] J Biol Chem. 2005 Apr 22;280(16):16157-62 [15718230.001]
  • [Cites] Neuropharmacology. 2005 Oct;49(5):687-94 [15992834.001]
  • [Cites] Cell Mol Life Sci. 2005 Aug;62(15):1724-33 [15990957.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11193-4 [14506299.001]
  • [Cites] Inorg Chem. 2004 Jun 28;43(13):3795-7 [15206857.001]
  • [Cites] J Alzheimers Dis. 2004 Jun;6(3):291-301 [15201484.001]
  • [Cites] Science. 1992 Apr 10;256(5054):184-5 [1566067.001]
  • [Cites] Int J Biochem Cell Biol. 2008;40(5):1030-42 [18160328.001]
  • [Cites] Science. 2001 Jun 22;292(5525):2251-2 [11424945.001]
  • [Cites] J Biol Chem. 2004 Dec 10;279(50):51958-64 [15465814.001]
  • [Cites] Neuron. 1996 May;16(5):921-32 [8630250.001]
  • [Cites] Biochim Biophys Acta. 2005 Jan 17;1703(2):149-56 [15680223.001]
  • [Cites] J Biol Chem. 2006 Jun 30;281(26):17670-80 [16648635.001]
  • [Cites] Cochrane Database Syst Rev. 2008 Jan 23;(1):CD005380 [18254079.001]
  • [Cites] Alzheimer Dis Assoc Disord. 2003 Jul-Sep;17(3):147-50 [14512827.001]
  • [Cites] Cell Mol Life Sci. 2000 May;57(5):705-15 [10892337.001]
  • [Cites] Biochem Soc Trans. 2005 Nov;33(Pt 5):1087-90 [16246051.001]
  • [Cites] Biochemistry. 2005 May 10;44(18):6776-87 [15865423.001]
  • [Cites] Int J Biochem Cell Biol. 2008;40(4):731-46 [18060826.001]
  • [Cites] Exp Neurol. 2005 Dec;196 (2):282-9 [16137679.001]
  • [Cites] J Neurol Sci. 1998 Jun 11;158(1):47-52 [9667777.001]
  • [Cites] J Biol Chem. 2002 Aug 30;277(35):32046-53 [12058030.001]
  • [Cites] Neurodegeneration. 1995 Mar;4(1):107-11 [7600179.001]
  • [Cites] Curr Drug Targets CNS Neurol Disord. 2002 Dec;1(6):567-74 [12769598.001]
  • [Cites] Ann N Y Acad Sci. 2004 Mar;1012:171-8 [15105264.001]
  • [Cites] Neurobiol Aging. 1999 May-Jun;20(3):325-30; discussion 339-42 [10588580.001]
  • [Cites] Neurobiol Aging. 2002 Nov-Dec;23(6):1031-8 [12470799.001]
  • [Cites] J Neurosci. 2006 May 31;26(22):6011-8 [16738244.001]
  • [Cites] Curr Opin Chem Biol. 2000 Apr;4(2):184-91 [10742195.001]
  • [Cites] Neuron. 2001 Jun;30(3):665-76 [11430801.001]
  • [Cites] J Biol Chem. 1998 May 22;273(21):12817-26 [9582309.001]
  • [Cites] Free Radic Biol Med. 2002 Dec 1;33(11):1475-9 [12446204.001]
  • [Cites] Arch Neurol. 2003 Dec;60(12):1685-91 [14676042.001]
  • [Cites] Mol Cancer Ther. 2006 Jul;5(7):1864-72 [16891473.001]
  • [Cites] Neurotoxicology. 2007 May;28(3):445-9 [17382398.001]
  • [Cites] Subcell Biochem. 2005;38:167-77 [15709478.001]
  • [Cites] J Neurol Sci. 2000 Feb 1;173(1):40-4 [10675578.001]
  • [Cites] J Mol Med (Berl). 2007 Apr;85(4):405-13 [17211610.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7317-9 [12032279.001]
  • [Cites] J Neurochem. 2000 Sep;75(3):1219-33 [10936205.001]
  • [Cites] Science. 1994 Sep 2;265(5177):1464-7 [8073293.001]
  • [Cites] Cochrane Database Syst Rev. 2006 Jan 25;(1):CD005380 [16437529.001]
  • [Cites] J Alzheimers Dis. 2004 Oct;6(5):515-25 [15505374.001]
  • [Cites] Biotechnol Bioeng. 2002 Oct 5;80(1):50-9 [12209786.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 16;102(33):11840-5 [16087879.001]
  • [Cites] Neuron. 2003 Mar 27;37(6):899-909 [12670420.001]
  • [Cites] Nature. 2006 Mar 16;440(7082):352-7 [16541076.001]
  • [Cites] J Alzheimers Dis. 2006 Nov;10(2-3):331-41 [17119296.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23223-8 [10438495.001]
  • [Cites] Eur J Biochem. 1997 Apr 15;245(2):355-63 [9151964.001]
  • [Cites] J Neurosci Res. 2007 Jan;85(1):213-22 [17061255.001]
  • [Cites] Br J Pharmacol. 2005 Dec;146(8):1041-59 [16205720.001]
  • (PMID = 18712494.001).
  • [ISSN] 1559-1174
  • [Journal-full-title] Neuromolecular medicine
  • [ISO-abbreviation] Neuromolecular Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Metals; 0 / Neurotoxins; 789U1901C5 / Copper; 7BHQ856EJ5 / Clioquinol; J41CSQ7QDS / Zinc
  •  go-up   go-down


75. Rath KS, Funk HM, Bowling MC, Richards WE, Drew AF: Expression of soluble interleukin-6 receptor in malignant ovarian tissue. Am J Obstet Gynecol; 2010 Sep;203(3):230.e1-8
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.
  • OBJECTIVE: The objective of the study was to investigate interleukin-6 receptor (IL6R) isoforms and sheddases in the ovarian tumor microenvironment.
  • Murine xenograft samples were tested by enzyme-linked immunosorbent assay to discriminate and evaluate tumor and host contributions of IL6R.
  • An in vivo xenograft model showed that host IL6R expression is also increased and regulated by tumor-associated inflammation.
  • Soluble IL6R may be an efficacious target for reducing IL6-mediated ovarian tumor progression.
  • [MeSH-minor] ADAM Proteins / metabolism. Adenocarcinoma, Clear Cell / metabolism. Adult. Aged. Amyloid Precursor Protein Secretases / metabolism. Animals. Cell Line, Tumor. Cystadenocarcinoma, Papillary / metabolism. Cystadenocarcinoma, Serous / metabolism. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunohistochemistry. Interleukin-6 / metabolism. Membrane Proteins / metabolism. Mice. Middle Aged. Ovary / metabolism. Polymerase Chain Reaction. Protein Isoforms. RNA / metabolism. Up-Regulation

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • 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
  • [Copyright] Copyright 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20471626.001).
  • [ISSN] 1097-6868
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Membrane Proteins; 0 / Protein Isoforms; 0 / Receptors, Interleukin-6; 63231-63-0 / RNA; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase; EC 3.4.24.81 / ADAM10 protein, human
  •  go-up   go-down


76. Fang B, Jia L, Jia J: Chinese Presenilin-1 V97L mutation enhanced Abeta42 levels in SH-SY5Y neuroblastoma cells. Neurosci Lett; 2006 Oct 2;406(1-2):33-7
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.
  • To verify whether this mutation is pathologically functional, we established mutation type and wild type Presenilin-1 gene stably transfected cell lines (human neuroblastoma SH-SY5Y cells) to detect beta-amyloid (Abeta) concentrations using ELISA and radioimmunity methods.
  • We also examined levels of beta-amyloid precursor protein cleaving enzyme (BACE) and amyloid precursor protein (APP) to explore their impact upon beta-amyloid production.
  • [MeSH-major] Alzheimer Disease / genetics. Amyloid beta-Peptides / biosynthesis. Amyloid beta-Protein Precursor / metabolism. Membrane Proteins / genetics. Mutation, Missense / genetics. Neurons / metabolism. Peptide Fragments / biosynthesis
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Asian Continental Ancestry Group / genetics. Aspartic Acid Endopeptidases. Brain / metabolism. Brain / physiopathology. Endopeptidases / metabolism. Extracellular Fluid / metabolism. Genetic Predisposition to Disease / genetics. Humans. Intracellular Fluid / metabolism. Neuroblastoma. Presenilin-1. Time Factors. Transfection. Tumor Cells, Cultured. Up-Regulation / genetics

  • Genetic Alliance. consumer health - Neuroblastoma.
  • Genetic Alliance. consumer health - Neuroblastoma 1.
  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16916581.001).
  • [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] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / Membrane Proteins; 0 / PSEN1 protein, human; 0 / Peptide Fragments; 0 / Presenilin-1; 0 / amyloid beta-protein (1-42); EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  •  go-up   go-down


77. Meng RD, Shelton CC, Li YM, Qin LX, Notterman D, Paty PB, Schwartz GK: gamma-Secretase inhibitors abrogate oxaliplatin-induced activation of the Notch-1 signaling pathway in colon cancer cells resulting in enhanced chemosensitivity. Cancer Res; 2009 Jan 15;69(2):573-82
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.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Organoplatinum Compounds / pharmacology. Receptor, Notch1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Cell Line, Tumor. Enzyme Activation. HCT116 Cells. HT29 Cells. Humans. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction / drug effects. Sulfonamides / pharmacology

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 2007 Apr 18;99(8):616-27 [17440163.001]
  • [Cites] Genes Dev. 2007 Mar 1;21(5):562-77 [17344417.001]
  • [Cites] Neurochem Res. 2007 Jun;32(6):1016-23 [17401676.001]
  • [Cites] Neoplasia. 2007 May;9(5):427-34 [17534448.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] Mol Cancer Ther. 2007 Jul;6(7):1983-92 [17604336.001]
  • [Cites] Oncologist. 2007 Aug;12(8):942-51 [17766653.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7954-9 [17804701.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):131-44 [18166351.001]
  • [Cites] Nature. 2008 Jan 3;451(7174):76-80 [18172499.001]
  • [Cites] Cell Oncol. 2008;30(1):1-11 [18219106.001]
  • [Cites] EMBO J. 2001 Jul 2;20(13):3427-36 [11432830.001]
  • [Cites] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031.001]
  • [Cites] Curr Biol. 2002 Jun 25;12(12):1006-11 [12123574.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] J Virol. 2003 Jun;77(12):7106-12 [12768030.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33445-9 [12815056.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2937-44 [14583609.001]
  • [Cites] Oncogene. 2004 Feb 5;23(5):1146-52 [14762442.001]
  • [Cites] Mol Cancer Ther. 2004 Feb;3(2):169-78 [14985457.001]
  • [Cites] Blood. 2004 May 1;103(9):3503-10 [14670925.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6854-7 [15466172.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7787-93 [15520184.001]
  • [Cites] Bioorg Med Chem Lett. 2005 Jan 17;15(2):373-8 [15603957.001]
  • [Cites] Br J Cancer. 2005 Feb 28;92(4):751-9 [15685243.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8530-7 [16166334.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6333-44 [15940249.001]
  • [Cites] Br J Cancer. 2005 Sep 19;93(6):709-18 [16136053.001]
  • [Cites] Mol Cancer Ther. 2005 Oct;4(10):1585-94 [16227409.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1517-25 [16452208.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2778-84 [16510599.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4182-90 [16618740.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4715-24 [16651424.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4147-53 [16857785.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Mol Cancer Ther. 2006 Jul;5(7):1883-94 [16891475.001]
  • [Cites] Int J Oncol. 2007 Jan;30(1):247-51 [17143535.001]
  • [Cites] Cell Death Differ. 2007 Jan;14(1):189-92 [16810324.001]
  • [Cites] Circ Res. 2007 Jan 5;100(1):70-8 [17158336.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Gynecol Oncol. 2007 Feb;104(2):352-61 [17098279.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1879-82 [17332312.001]
  • [Cites] Cell Death Differ. 2007 May;14(5):982-91 [17186020.001]
  • (PMID = 19147571.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009207; United States / NCI NIH HHS / CA / T32 CA009207-35
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NOTCH1 protein, human; 0 / Organoplatinum Compounds; 0 / Receptor, Notch1; 0 / Sulfonamides; 04ZR38536J / oxaliplatin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS324521; NLM/ PMC3242515
  •  go-up   go-down


78. Maretzky T, Reiss K, Ludwig A, Buchholz J, Scholz F, Proksch E, de Strooper B, Hartmann D, Saftig P: ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and beta-catenin translocation. Proc Natl Acad Sci U S A; 2005 Jun 28;102(26):9182-7
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.
  • [MeSH-minor] ADAM Proteins. Amyloid Precursor Protein Secretases. Animals. Blotting, Western. Cell Adhesion. Cell Line, Tumor. Cell Movement. Cell Proliferation. Cyclin D1 / metabolism. Down-Regulation. Embryo, Mammalian / metabolism. Fibroblasts / metabolism. Genetic Vectors. Humans. Keratinocytes / metabolism. Mice. Protein Binding. Protein Structure, Tertiary. Protein Transport. RNA Interference. Signal Transduction. Transfection. Wound Healing. beta Catenin


79. Hoozemans JJ, Stieler J, van Haastert ES, Veerhuis R, Rozemuller AJ, Baas F, Eikelenboom P, Arendt T, Scheper W: The unfolded protein response affects neuronal cell cycle protein expression: implications for Alzheimer's disease pathogenesis. Exp Gerontol; 2006 Apr;41(4):380-6
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.
  • In this study we show that the protein levels of BiP/GRP78, an ER-stress marker, is increased in Braak stages B and C for amyloid deposits.
  • This is in contrast to the levels of cell cycle markers cyclin D1, cyclin E and phosphorylated retinoblastoma protein (ppRb) which are decreased in Braak stage C compared to Braak stage A for amyloid deposits.
  • [MeSH-minor] Biomarkers / analysis. Blotting, Western / methods. Cell Cycle. Cell Differentiation. Cyclin D. Cyclin E / analysis. Cyclin E / metabolism. Cyclins / analysis. Cyclins / metabolism. Endoplasmic Reticulum / metabolism. Endoplasmic Reticulum / pathology. Flow Cytometry. Heat-Shock Proteins / analysis. Humans. Immunohistochemistry / methods. Molecular Chaperones / analysis. Neuroblastoma. Phosphorylation. Retinoblastoma Protein / analysis. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16564150.001).
  • [ISSN] 0531-5565
  • [Journal-full-title] Experimental gerontology
  • [ISO-abbreviation] Exp. Gerontol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cell Cycle Proteins; 0 / Cyclin D; 0 / Cyclin E; 0 / Cyclins; 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / Retinoblastoma Protein; 0 / molecular chaperone GRP78
  •  go-up   go-down


80. Shen S, Callaghan D, Juzwik C, Xiong H, Huang P, Zhang W: ABCG2 reduces ROS-mediated toxicity and inflammation: a potential role in Alzheimer's disease. J Neurochem; 2010 Sep;114(6):1590-604
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.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Amyloid beta-Peptides / metabolism. Amyloid beta-Protein Precursor / metabolism. Animals. Brain / metabolism. Cell Line. Cell Line, Tumor. Cell Survival. Chemokine CXCL1 / biosynthesis. Chemokine CXCL2 / biosynthesis. Hemin / metabolism. Humans. Hydrogen Peroxide / toxicity. Inflammation / metabolism. Interleukin-8 / biosynthesis. Mice. Mice, Knockout. NF-kappa B / metabolism. Peptide Fragments / metabolism. tert-Butylhydroperoxide / toxicity

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • Hazardous Substances Data Bank. TERT-BUTYL HYDROPEROXIDE .
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • 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
  • [Copyright] © 2010 National Research Council of Canada. Journal Compilation © 2010 International Society for Neurochemistry.
  • (PMID = 20626554.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Abcg2 protein, mouse; 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / CXCL2 protein, human; 0 / Chemokine CXCL1; 0 / Chemokine CXCL2; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Reactive Oxygen Species; 0 / amyloid beta-protein (1-40); 743LRP9S7N / Hemin; 955VYL842B / tert-Butylhydroperoxide; BBX060AN9V / Hydrogen Peroxide
  •  go-up   go-down


81. Ohyagi Y, Tabira T: Intracellular amyloid beta-protein and its associated molecules in the pathogenesis of Alzheimer's disease. Mini Rev Med Chem; 2006 Oct;6(10):1075-80
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] Intracellular amyloid beta-protein and its associated molecules in the pathogenesis of Alzheimer's disease.
  • Amyloid beta-protein (Abeta) plays a pivotal role in Alzheimer's disease (AD).
  • [MeSH-major] Alzheimer Disease / genetics. Alzheimer Disease / physiopathology. Amyloid beta-Peptides / metabolism. Intracellular Space / metabolism. Peptide Fragments / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis / physiology. Humans. Molecular Sequence Data. Neurons / metabolism. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17073707.001).
  • [ISSN] 1389-5575
  • [Journal-full-title] Mini reviews in medicinal chemistry
  • [ISO-abbreviation] Mini Rev Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (1-42)
  • [Number-of-references] 65
  •  go-up   go-down


82. Magy N, Grateau G: [Tenth International Symposium on Amyloid and Amyloidosis]. Rev Med Interne; 2005 Feb;26(2):167-71
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] [Tenth International Symposium on Amyloid and Amyloidosis].
  • [Transliterated title] Compte rendu du "Tenth International Symposium on Amyloid and Amyloidosis", Tours 18-22 avril 2004.

  • Genetic Alliance. consumer health - Amyloidosis.
  • MedlinePlus Health Information. consumer health - Amyloidosis.
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. Etanercept .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15770789.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Comparative Study; Congresses
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Amyloid; 0 / Antineoplastic Agents, Alkylating; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Receptors, Tumor Necrosis Factor; 0 / Serum Amyloid A Protein; OP401G7OJC / Etanercept; Q41OR9510P / Melphalan
  •  go-up   go-down


83. Ito S, Ueno T, Ohtsuki S, Terasaki T: Lack of brain-to-blood efflux transport activity of low-density lipoprotein receptor-related protein-1 (LRP-1) for amyloid-beta peptide(1-40) in mouse: involvement of an LRP-1-independent pathway. J Neurochem; 2010 Jun;113(5):1356-63
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] Lack of brain-to-blood efflux transport activity of low-density lipoprotein receptor-related protein-1 (LRP-1) for amyloid-beta peptide(1-40) in mouse: involvement of an LRP-1-independent pathway.
  • The contribution of low-density lipoprotein receptor-related protein-1 (LRP-1) to the brain-to-blood amyloid-beta peptide (A beta) efflux transport across the blood-brain barrier (BBB) remains controversial.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Blood-Brain Barrier / physiology. Peptide Fragments / metabolism. Signal Transduction / physiology. Tumor Suppressor Proteins / pharmacology

  • Hazardous Substances Data Bank. METHYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20367755.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Indicators and Reagents; 0 / Iodine Radioisotopes; 0 / Lrp1 protein, mouse; 0 / Methylamines; 0 / Peptide Fragments; 0 / Receptors, LDL; 0 / Tumor Suppressor Proteins; 0 / alpha-Macroglobulins; 0 / amyloid beta-protein (1-40); BSF23SJ79E / methylamine
  •  go-up   go-down


84. van Rooijen M, Hansson LO, Frostegård J, Silveira A, Hamsten A, Bremme K: Treatment with combined oral contraceptives induces a rise in serum C-reactive protein in the absence of a general inflammatory response. J Thromb Haemost; 2006 Jan;4(1):77-82
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.
  • Serum levels of CRP, serum amyloid A (SAA), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), antibodies against oxidized LDL, insulin and insulin-like growth factor-I (IGF-I) along with insulin-like growth factor binding protein-1 (IGFBP-1) and IGFBP-3 were analyzed before and during the two treatments.

  • 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 = 16409455.001).
  • [ISSN] 1538-7933
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Contraceptives, Oral, Combined; 9007-41-4 / C-Reactive Protein
  •  go-up   go-down


85. Huang Y, Erdmann N, Peng H, Zhao Y, Zheng J: The role of TNF related apoptosis-inducing ligand in neurodegenerative diseases. Cell Mol Immunol; 2005 Apr;2(2):113-22
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.
  • As one member of a death ligand family, TRAIL was originally thought to target only tumor cells and was not present in CNS.
  • TRAIL is also induced on neuron by beta-amyloid protein, an important pathogen for Alzheimer's disease.
  • [MeSH-major] Apoptosis Regulatory Proteins / physiology. Membrane Glycoproteins / physiology. Neurodegenerative Diseases / pathology. Neurodegenerative Diseases / physiopathology. Tumor Necrosis Factor-alpha / physiology

  • MedlinePlus Health Information. consumer health - Degenerative Nerve Diseases.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16191417.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P01 NS043985; United States / NCRR NIH HHS / RR / P20 RR15635; United States / NINDS NIH HHS / NS / R01 NS 41858
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 113
  •  go-up   go-down


86. Maezawa I, Hong HS, Wu HC, Battina SK, Rana S, Iwamoto T, Radke GA, Pettersson E, Martin GM, Hua DH, Jin LW: A novel tricyclic pyrone compound ameliorates cell death associated with intracellular amyloid-beta oligomeric complexes. J Neurochem; 2006 Jul;98(1):57-67
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] A novel tricyclic pyrone compound ameliorates cell death associated with intracellular amyloid-beta oligomeric complexes.
  • The neurotoxicity of amyloid-beta protein (Abeta) is widely regarded as one of the fundamental causes of neurodegeneration in Alzheimer's disease (AD).
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Amyloid beta-Peptides / toxicity. Intracellular Space / drug effects. Neuroprotective Agents / pharmacology. Pyrones / pharmacology
  • [MeSH-minor] Carbamates / pharmacology. Cell Count / methods. Cell Death / drug effects. Cell Line, Tumor. Dipeptides / pharmacology. Dose-Response Relationship, Drug. Drug Interactions. Enzyme-Linked Immunosorbent Assay / methods. Fluorescent Antibody Technique / methods. Humans. Microscopy, Atomic Force / methods. Neuroblastoma / pathology. Surface Plasmon Resonance / methods. Time Factors

  • 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 = 16805796.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG19711; United States / NCI NIH HHS / CA / CA86842
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / CP2 compound; 0 / Carbamates; 0 / Dipeptides; 0 / L 685458; 0 / Neuroprotective Agents; 0 / Pyrones
  •  go-up   go-down


87. Salaita K, Nair PM, Petit RS, Neve RM, Das D, Gray JW, Groves JT: Restriction of receptor movement alters cellular response: physical force sensing by EphA2. Science; 2010 Mar 12;327(5971):1380-5
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.
  • [Title] Restriction of receptor movement alters cellular response: physical force sensing by EphA2.
  • Activation of the EphA2 receptor tyrosine kinase by ephrin-A1 ligands presented on apposed cell surfaces plays important roles in development and exhibits poorly understood functional alterations in cancer.
  • We reconstituted this intermembrane signaling geometry between live EphA2-expressing human breast cancer cells and supported membranes displaying laterally mobile ephrin-A1.
  • Receptor-ligand binding, clustering, and subsequent lateral transport within this junction were observed.
  • EphA2 transport can be blocked by physical barriers nanofabricated onto the underlying substrate.
  • This physical reorganization of EphA2 alters the cellular response to ephrin-A1, as observed by changes in cytoskeleton morphology and recruitment of a disintegrin and metalloprotease 10.
  • Quantitative analysis of receptor-ligand spatial organization across a library of 26 mammary epithelial cell lines reveals characteristic differences that strongly correlate with invasion potential.
  • These observations reveal a mechanism for spatio-mechanical regulation of EphA2 signaling pathways.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Cell Biol. 2002 Aug;4(8):565-73 [12134157.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Jul;3(7):475-86 [12094214.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Jan;4(1):33-45 [12511867.001]
  • [Cites] Nat Rev Cancer. 2003 May;3(5):362-74 [12724734.001]
  • [Cites] Genome Biol. 2003;4(5):P3 [12734009.001]
  • [Cites] Nat Neurosci. 2004 May;7(5):501-9 [15107857.001]
  • [Cites] J Cell Sci. 1985 Apr;75:279-301 [3900106.001]
  • [Cites] Science. 1994 Nov 4;266(5186):816-9 [7973638.001]
  • [Cites] Science. 1997 Jan 31;275(5300):651-3 [9005848.001]
  • [Cites] Cell. 2005 Apr 8;121(1):127-39 [15820684.001]
  • [Cites] J Biol Chem. 2005 Jul 15;280(28):26526-32 [15901737.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):111-8 [16098464.001]
  • [Cites] Cell. 2005 Oct 21;123(2):291-304 [16239146.001]
  • [Cites] Science. 2005 Nov 18;310(5751):1139-43 [16293750.001]
  • [Cites] Science. 2005 Nov 18;310(5751):1191-3 [16293763.001]
  • [Cites] Chembiochem. 2006 Mar;7(3):436-40 [16456901.001]
  • [Cites] J Cell Sci. 2006 Oct 1;119(Pt 19):3901-3 [16988024.001]
  • [Cites] Science. 2006 Oct 13;314(5797):298-300 [17038622.001]
  • [Cites] Curr Opin Chem Biol. 2006 Dec;10(6):544-50 [17070724.001]
  • [Cites] Cancer Cell. 2006 Dec;10(6):515-27 [17157791.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):659-72 [17721431.001]
  • [Cites] Nat Mater. 2007 Dec;6(12):997-1003 [17891143.001]
  • [Cites] Sci Signal. 2008;1(15):re2 [18413883.001]
  • [Cites] Nat Cell Biol. 2008 Aug;10(8):955-63 [18641640.001]
  • [Cites] Biophys J. 2008 Sep;95(5):2512-9 [18515392.001]
  • [Cites] J Cell Sci. 2008 Oct 15;121(Pt 20):3285-92 [18843115.001]
  • [Cites] Biophys J. 2008 Dec;95(11):5374-84 [18775961.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):108-22 [19165226.001]
  • [Cites] Am J Pathol. 2009 Apr;174(4):1492-503 [19264906.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12729-34 [19622735.001]
  • [Cites] Science. 2009 Nov 27;326(5957):1205 [19965460.001]
  • [Cites] Science. 2009 Nov 27;326(5957):1216-9 [19965464.001]
  • [Cites] Science. 2009 Nov 27;326(5957):1220-4 [19965465.001]
  • [Cites] Mol Cancer Res. 2002 Nov;1(1):79-87 [12496371.001]
  • [Cites] Acc Chem Res. 2002 Mar;35(3):149-57 [11900518.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6548-53 [11371622.001]
  • [Cites] Nature. 2001 Dec 20-27;414(6866):933-8 [11780069.001]
  • [CommentIn] Nat Rev Mol Cell Biol. 2010 May;11(5):311 [20419888.001]
  • [CommentIn] Science. 2010 Mar 12;327(5971):1335-6 [20223974.001]
  • (PMID = 20223987.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA143836-01; United States / NCI NIH HHS / CA / CA058207-060002; United States / NCI NIH HHS / CA / P50 CA058207-060002; United States / NCI NIH HHS / CA / P50 CA058207-08; United States / NCI NIH HHS / CA / U54 CA143836; United States / NCI NIH HHS / CA / CA058207-09; United States / NCI NIH HHS / CA / U54 CA 112970; United States / NCI NIH HHS / CA / P50 CA 58207; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / U54 CA112970; United States / NCI NIH HHS / CA / P50 CA058207-09; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / U54 CA112970-01; United States / NCI NIH HHS / CA / CA058207-08; United States / NCI NIH HHS / CA / CA112970-01; United States / NCI NIH HHS / CA / CA143836-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / Ephrin-A1; 0 / Ligands; 0 / Lipid Bilayers; 0 / Membrane Proteins; 9013-26-7 / Actomyosin; EC 2.7.10.1 / Receptor, EphA2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
  • [Other-IDs] NLM/ NIHMS192048; NLM/ PMC2895569
  •  go-up   go-down


88. Farnie G, Clarke RB: Mammary stem cells and breast cancer--role of Notch signalling. Stem Cell Rev; 2007 Jun;3(2):169-75
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.
  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Animals. Antigens, CD24 / metabolism. Antigens, CD44 / metabolism. Biomarkers, Tumor / metabolism. Dipeptides / pharmacology. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation, Neoplastic. Humans. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Mammary Neoplasms, Experimental / metabolism. Mammary Neoplasms, Experimental / pathology. Mammary Neoplasms, Experimental / prevention & control. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / prevention & control. Neoplasm Transplantation. Spheroids, Cellular / metabolism. Spheroids, Cellular / pathology. Up-Regulation