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  • Male  (3)
  • 2000-2004  (3)
  • 1965-1969
  • 1955-1959
  • 1945-1949
  • 1
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    An essential role of N-terminal arginylation in cardiovascular development (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: The enzymatic conjugation of arginine to the N-termini of proteins is a part of the ubiquitin-dependent N-end rule pathway of protein degradation. In mammals, three N-terminal residues-aspartate, glutamate, and cysteine-are substrates for arginylation. The mouse ATE1 gene encodes a family of Arg-tRNA-protein transferases (R-transferases) that mediate N-terminal arginylation. We constructed ATE1-lacking mouse strains and found that ATE1-/- embryos die with defects in heart development and in angiogenic remodeling of the early vascular plexus. Through biochemical analyses, we show that N-terminal cysteine, in contrast to N-terminal aspartate and glutamate, is oxidized before its arginylation by R-transferase, suggesting that the arginylation branch of the N-end rule pathway functions as an oxygen sensor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Yong Tae -- Kashina, Anna S -- Davydov, Ilia V -- Hu, Rong-Gui -- An, Jee Young -- Seo, Jai Wha -- Du, Fangyong -- Varshavsky, Alexander -- GM31530/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):96-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, 147-75, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098698" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylation ; Aminoacyltransferases/*genetics/*metabolism ; Animals ; Aorta/embryology ; Arginine/*metabolism ; Aspartic Acid/metabolism ; Blood Vessels/*embryology ; Cell Line ; Cysteic Acid/metabolism ; Cysteine/metabolism ; Female ; Glutamic Acid/metabolism ; Heart/*embryology ; Heart Defects, Congenital/embryology ; Heart Septal Defects/embryology ; Hypoxia-Inducible Factor 1, alpha Subunit ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic ; Oxidation-Reduction ; Proteins/*metabolism ; Pulmonary Artery/embryology ; RGS Proteins/metabolism ; Recombinant Proteins/metabolism ; Sulfinic Acids/metabolism ; Transcription Factors/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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  • 2
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    A human genome diversity cell line panel (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cann, Howard M -- de Toma, Claudia -- Cazes, Lucien -- Legrand, Marie-Fernande -- Morel, Valerie -- Piouffre, Laurence -- Bodmer, Julia -- Bodmer, Walter F -- Bonne-Tamir, Batsheva -- Cambon-Thomsen, Anne -- Chen, Zhu -- Chu, J -- Carcassi, Carlo -- Contu, Licinio -- Du, Ruofu -- Excoffier, Laurent -- Ferrara, G B -- Friedlaender, Jonathan S -- Groot, Helena -- Gurwitz, David -- Jenkins, Trefor -- Herrera, Rene J -- Huang, Xiaoyi -- Kidd, Judith -- Kidd, Kenneth K -- Langaney, Andre -- Lin, Alice A -- Mehdi, S Qasim -- Parham, Peter -- Piazza, Alberto -- Pistillo, Maria Pia -- Qian, Yaping -- Shu, Qunfang -- Xu, Jiujin -- Zhu, S -- Weber, James L -- Greely, Henry T -- Feldman, Marcus W -- Thomas, Gilles -- Dausset, Jean -- Cavalli-Sforza, L Luca -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):261-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11954565" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Specimen Banks ; *Cell Line ; Continental Population Groups/genetics ; DNA/genetics ; Databases, Factual ; Female ; *Genetic Variation ; *Genome, Human ; Haplotypes ; Humans ; Informed Consent ; *Lymphocytes ; Male ; Polymorphism, Single Nucleotide
    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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  • 3
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    TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Insulin resistance is a major hallmark in the development of type II diabetes, which is characterized by the failure of insulin to promote glucose uptake in muscle and to suppress glucose production in liver. The serine-threonine kinase Akt (PKB) is a principal target of insulin signaling that inhibits hepatic glucose output when glucose is available from food. Here we show that TRB3, a mammalian homolog of Drosophila tribbles, functions as a negative modulator of Akt. TRB3 expression is induced in liver under fasting conditions, and TRB3 disrupts insulin signaling by binding directly to Akt and blocking activation of the kinase. Amounts of TRB3 RNA and protein were increased in livers of db/db diabetic mice compared with those in wild-type mice. Hepatic overexpression of TRB3 in amounts comparable to those in db/db mice promoted hyperglycemia and glucose intolerance. Our results suggest that, by interfering with Akt activation, TRB3 contributes to insulin resistance in individuals with susceptibility to type II diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Keyong -- Herzig, Stephan -- Kulkarni, Rohit N -- Montminy, Marc -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791994" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Diabetes Mellitus/genetics/metabolism ; Enzyme Activation ; Fasting ; Genetic Vectors ; Glucose/metabolism ; Glucose Intolerance ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/pharmacology ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; RNA Interference ; Rats ; Repressor Proteins ; Signal Transduction ; Transfection ; Transgenes ; Tumor Cells, Cultured ; Two-Hybrid System Techniques
    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)
    Location Call Number Expected Availability
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