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  • 1
    Electronic Resource
    Electronic Resource
    Cascade of autophosphorylation in the β-subunit of the insulin receptor (1989)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 39 (1989), S. 429-441 
    Details
    ISSN: 0730-2312
    Keywords: transmembrane signal ; protein phosphorylation ; tyrosine kinase ; signal transmission ; phosphorylation cascade ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin stimulated autophosphorylation of the β-subunit of the insulin receptor purified from Fao hepatoma cells or purified from Chinese hamster ovary (CHO/HIRC) or Swiss 3T3 (3T3/HIRC) cells transfected with the wild-type human insulin receptor cDNA. Autophosphorylation of the purified receptor occurred in at least two regions of the β-subunit: the regulatory region containing Tyr-1146, Tyr-1150, and Tyr-1151, and the C-terminus containing Tyr-1316 and Tyr-1322. In the presence of antiphosphotyrosine antibody (α-PY), autophosphorylation of the purified receptor was inhibited nearly 80% during insulin stimulation. Tryptic peptide mapping showed that α-PY inhibited autophosphorylation of both tyrosyl residues in the C-terminus and one tyrosyl residue in the regulatory region, either Tyr-1150 or Tyr-1151. Thus, a bis-phosphorylated form of the regulatory region accumulated in the presence of α-PY, which contained Tyr(P)-1146 and either Tyr(P)-1150 or 1151. In intact Fao, CHO/HIRC, and 3T3/HIRC cells, insulin stimulated tyrosyl phosphorylation of the β-subunit of the insulin receptor. Tryptic peptide mapping indicated that the regulatory region of the β-subunit was mainly (〉80%) bis-phosphorylated; however, all three tyrosyl residues of the regulatory region were phosphorylated in about 20% of the receptors. As the phosphotransferase was activated by tris-phosphorylation but not bis-phosphorylation of the regulatory region of the β-subunit (White et al.: Journal of Biological Chemistry 263:2969-2980, 1988), the extent of autophosphorylation in the regulatory region may play an important regulatory role during signal transmission in the intact cell.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240390409
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  • 2
    Electronic Resource
    Electronic Resource
    Phosphorylation of the solubilized insulin receptor by the gene product of the Rous sarcoma virus, pp60src (1984)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 26 (1984), S. 169-179 
    Details
    ISSN: 0730-2312
    Keywords: insulin receptor ; tyrosine kinase ; pp60src ; phosphorylation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Both the insulin receptor and the gene product of the Rous sarcoma virus, pp60src, are protein kinases which phosphorylate themselves and other proteins on tyrosinc residues. Addition of the solubilized insulin receptor to purified pp60src increased the phosphorylation of the β-subunit of the insulin receptor. Phosphorylation of the insulin receptor by pp60src occurred both in the absence and presence of insulin but did not alter the insulin dose response for autophosphorylation of the receptor. Increasing concentrations of pp60src increased the phosphorylation of the receptor and at high concentrations equaled the maximal effect produced by insulin. Our observations suggest a possible mechanism by which the metabolically regulated insulin receptor tyrosine kinase could be altered by other tyrosine kinases such as that associated with pp60src. Further studies will be required to determine if the insulin receptor is phosphorylated by pp60src in Rous sarcoma virus-infected cells.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240260305
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  • 3
    Electronic Resource
    Electronic Resource
    Phosphorylation of glycolytic and gluconeogenic enzymes by the insulin receptor kinase (1987)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 33 (1987), S. 15-26 
    Details
    ISSN: 0730-2312
    Keywords: phosphorylation ; insulin receptor ; tyrosine kinase ; phosphofructokinase ; glycolysis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Various glycolytic and gluconeogenic enzymes were tested as substrates for the insulin receptor kinase. Phosphofructokinase and phosphoglycerate mutase were found to be the best substrates. Phosphorylation of these enzymes was rapid, stimulated 2- to 6-fold by 10-7 M insulin and occurred exclusively on tyrosine residues. Enolase, fructose 1,6-bisphosphatase, lactate dehydrogenases in decreasing order, were also subject to insulin-stimulated phosphorylation but to a smaller extent than that for phpsphofructokinase or phosphoglycerate mutase.The phosphorylation of phosphofructokinase was studied most extensively since phosphofructokinase is known to catalyze a rate-limiting step in glycolosis. The apparent Km of the insulin receptor for phosphofructokinase was 0.1 μM, which is within the physiologic range of concentration of this enzyme in most cells. Tyrosine phosphorylation of phosphofructokinase paralleled autophosphorylation of the β-subunit of the insulin receptor with respect to time course, insulin dose response (half maximal effect between 10-9 and 10-8 M insulin), and cation requirement (Mn2+ 〉 Mg2+ 〉 〉 Ca2+). Further study will be required to determine whether the tyrosine phosphorylation of phosphofructokinase plays a role in insulin-stimulated increases in glycolytic flux.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240330103
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  • 4
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    Smallpox transmission risks: how bad? (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahn, Laura H -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):50-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12102091" target="_blank"〉PubMed〈/a〉
    Keywords: *Air Microbiology ; Bioterrorism ; Disease Outbreaks ; Humans ; New York City/epidemiology ; Policy Making ; Smallpox/epidemiology/*transmission ; USSR/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease. Abeta generation depends on proteolytic cleavage of the amyloid precursor protein (APP) by two unknown proteases: beta-secretase and gamma-secretase. These proteases are prime therapeutic targets. A transmembrane aspartic protease with all the known characteristics of beta-secretase was cloned and characterized. Overexpression of this protease, termed BACE (for beta-site APP-cleaving enzyme) increased the amount of beta-secretase cleavage products, and these were cleaved exactly and only at known beta-secretase positions. Antisense inhibition of endogenous BACE messenger RNA decreased the amount of beta-secretase cleavage products, and purified BACE protein cleaved APP-derived substrates with the same sequence specificity as beta-secretase. Finally, the expression pattern and subcellular localization of BACE were consistent with that expected for beta-secretase. Future development of BACE inhibitors may prove beneficial for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassar, R -- Bennett, B D -- Babu-Khan, S -- Kahn, S -- Mendiaz, E A -- Denis, P -- Teplow, D B -- Ross, S -- Amarante, P -- Loeloff, R -- Luo, Y -- Fisher, S -- Fuller, J -- Edenson, S -- Lile, J -- Jarosinski, M A -- Biere, A L -- Curran, E -- Burgess, T -- Louis, J C -- Collins, F -- Treanor, J -- Rogers, G -- Citron, M -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):735-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen, Inc., One Amgen Center Drive, M/S 29-2-B, Thousand Oaks, CA 91320-1799, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531052" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/*enzymology ; Amino Acid Motifs ; Amino Acid Sequence ; Amyloid Precursor Protein Secretases ; Amyloid beta-Peptides/*biosynthesis ; Amyloid beta-Protein Precursor/*metabolism ; Animals ; Aspartic Acid Endopeptidases/chemistry/genetics/*isolation & ; purification/*metabolism ; Binding Sites ; Brain/enzymology/metabolism ; Cell Line ; Cloning, Molecular ; Endopeptidases ; Endosomes/enzymology ; Gene Expression ; Gene Library ; Golgi Apparatus/enzymology ; Humans ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Peptides/metabolism ; Protease Inhibitors/pharmacology ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Privacy in genetics research (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuller, B P -- Kahn, M J -- Barr, P A -- Biesecker, L -- Crowley, E -- Garber, J -- Mansoura, M K -- Murphy, P -- Murray, J -- Phillips, J -- Rothenberg, K -- Rothstein, M -- Stopfer, J -- Swergold, G -- Weber, B -- Collins, F K -- Hudson, K L -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1359-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉barbaraf@exchange.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490410" target="_blank"〉PubMed〈/a〉
    Keywords: *Bioethics ; *Confidentiality ; *Disclosure ; Ethics Committees, Research ; Federal Government ; *Genetic Privacy ; *Genetic Research ; *Genetics, Medical ; Government Regulation ; Humans ; Informed Consent ; Privacy ; Research/legislation & jurisprudence/*standards ; *Research Subjects ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Tumstatin, an endothelial cell-specific inhibitor of protein synthesis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: Tumstatin is a 28-kilodalton fragment of type IV collagen that displays both anti-angiogenic and proapoptotic activity. Here we show that tumstatin functions as an endothelial cell-specific inhibitor of protein synthesis. Through a requisite interaction with alphaVbeta3 integrin, tumstatin inhibits activation of focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3-kinase), protein kinase B (PKB/Akt), and mammalian target of rapamycin (mTOR), and it prevents the dissociation of eukaryotic initiation factor 4E protein (eIF4E) from 4E-binding protein 1. These results establish a role for integrins in mediating cell-specific inhibition of cap-dependent protein synthesis and suggest a potential mechanism for tumstatin's selective effects on endothelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeshima, Yohei -- Sudhakar, Akulapalli -- Lively, Julie C -- Ueki, Kohjiro -- Kharbanda, Surender -- Kahn, C Ronald -- Sonenberg, Nahum -- Hynes, Richard O -- Kalluri, Raghu -- DK-51711/DK/NIDDK NIH HHS/ -- DK-55001/DK/NIDDK NIH HHS/ -- P01-HL66105/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Matrix Biology, Department of Medicine and the Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778052" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Autoantigens/chemistry/metabolism/*pharmacology ; Carrier Proteins/metabolism ; Cattle ; Cells, Cultured ; Collagen Type IV/chemistry/metabolism/*pharmacology ; Endothelium, Vascular/*cytology/drug effects/*metabolism ; Enzyme Activation/drug effects ; Eukaryotic Initiation Factor-4E ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Humans ; Mice ; Molecular Sequence Data ; Peptide Fragments/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; *Protein Biosynthesis/drug effects ; Protein Kinase Inhibitors ; Protein Kinases/metabolism ; Protein Synthesis Inhibitors/*pharmacology ; *Protein-Serine-Threonine Kinases ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; RNA Caps/metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Vitronectin/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    Molecular defects in insulin action (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahn, C R -- Goldstein, B J -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2662406" target="_blank"〉PubMed〈/a〉
    Keywords: Diabetes Mellitus/*physiopathology ; Humans ; Insulin/*physiology ; Insulin Resistance
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    SIRT3 regulates mitochondrial fatty-acid oxidation by reversible enzyme deacetylation (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-06
    Description: Sirtuins are NAD(+)-dependent protein deacetylases. They mediate adaptive responses to a variety of stresses, including calorie restriction and metabolic stress. Sirtuin 3 (SIRT3) is localized in the mitochondrial matrix, where it regulates the acetylation levels of metabolic enzymes, including acetyl coenzyme A synthetase 2 (refs 1, 2). Mice lacking both Sirt3 alleles appear phenotypically normal under basal conditions, but show marked hyperacetylation of several mitochondrial proteins. Here we report that SIRT3 expression is upregulated during fasting in liver and brown adipose tissues. During fasting, livers from mice lacking SIRT3 had higher levels of fatty-acid oxidation intermediate products and triglycerides, associated with decreased levels of fatty-acid oxidation, compared to livers from wild-type mice. Mass spectrometry of mitochondrial proteins shows that long-chain acyl coenzyme A dehydrogenase (LCAD) is hyperacetylated at lysine 42 in the absence of SIRT3. LCAD is deacetylated in wild-type mice under fasted conditions and by SIRT3 in vitro and in vivo; and hyperacetylation of LCAD reduces its enzymatic activity. Mice lacking SIRT3 exhibit hallmarks of fatty-acid oxidation disorders during fasting, including reduced ATP levels and intolerance to cold exposure. These findings identify acetylation as a novel regulatory mechanism for mitochondrial fatty-acid oxidation and demonstrate that SIRT3 modulates mitochondrial intermediary metabolism and fatty-acid use during fasting.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841477/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841477/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirschey, Matthew D -- Shimazu, Tadahiro -- Goetzman, Eric -- Jing, Enxuan -- Schwer, Bjoern -- Lombard, David B -- Grueter, Carrie A -- Harris, Charles -- Biddinger, Sudha -- Ilkayeva, Olga R -- Stevens, Robert D -- Li, Yu -- Saha, Asish K -- Ruderman, Neil B -- Bain, James R -- Newgard, Christopher B -- Farese, Robert V Jr -- Alt, Frederick W -- Kahn, C Ronald -- Verdin, Eric -- DK019514-29/DK/NIDDK NIH HHS/ -- DK59637/DK/NIDDK NIH HHS/ -- K01 DK076573/DK/NIDDK NIH HHS/ -- K08 AG022325/AG/NIA NIH HHS/ -- K08 AG022325-01A1/AG/NIA NIH HHS/ -- P01 HL068758/HL/NHLBI NIH HHS/ -- P01 HL068758-06A1/HL/NHLBI NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- P30 DK026743-26A1/DK/NIDDK NIH HHS/ -- R01 DK019514/DK/NIDDK NIH HHS/ -- R01 DK019514-29/DK/NIDDK NIH HHS/ -- R01 DK067509/DK/NIDDK NIH HHS/ -- R01 DK067509-04/DK/NIDDK NIH HHS/ -- U24 DK059637/DK/NIDDK NIH HHS/ -- U24 DK059637-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Mar 4;464(7285):121-5. doi: 10.1038/nature08778.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203611" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acyl-CoA Dehydrogenase, Long-Chain/chemistry/*metabolism ; Adenosine Triphosphate/biosynthesis/metabolism ; Adipose Tissue, Brown/enzymology/metabolism ; Animals ; Body Temperature Regulation ; Caloric Restriction ; Carnitine/analogs & derivatives/metabolism ; Cell Line ; Cold Temperature ; Fasting/metabolism ; Fatty Acids/*metabolism ; Humans ; Hypoglycemia/metabolism ; Liver/enzymology/metabolism ; Male ; Mass Spectrometry ; Mice ; Mitochondria/*enzymology/*metabolism ; Oxidation-Reduction ; Sirtuin 3/deficiency/genetics/*metabolism ; Triglycerides/metabolism ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Germany's gene law begins to bite (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahn, Patricia -- New York, N.Y. -- Science. 1992 Jan 31;255(5044):524-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11642978" target="_blank"〉PubMed〈/a〉
    Keywords: Attitude ; Containment of Biohazards ; *DNA, Recombinant ; Genetic Engineering ; Germany ; *Government Regulation ; Humans ; *Legislation as Topic ; Politics ; Public Opinion ; Research Personnel ; *Social Control, Formal
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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