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  • 1
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    Regulation of neuronal survival by the serine-threonine protein kinase Akt (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: A signaling pathway was delineated by which insulin-like growth factor 1 (IGF-1) promotes the survival of cerebellar neurons. IGF-1 activation of phosphoinositide 3-kinase (PI3-K) triggered the activation of two protein kinases, the serine-threonine kinase Akt and the p70 ribosomal protein S6 kinase (p70(S6K)). Experiments with pharmacological inhibitors, as well as expression of wild-type and dominant-inhibitory forms of Akt, demonstrated that Akt but not p70(S6K) mediates PI3-K-dependent survival. These findings suggest that in the developing nervous system, Akt is a critical mediator of growth factor-induced neuronal survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudek, H -- Datta, S R -- Franke, T F -- Birnbaum, M J -- Yao, R -- Cooper, G M -- Segal, R A -- Kaplan, D R -- Greenberg, M E -- DK39519/DK/NIDDK NIH HHS/ -- R01 CA18689/CA/NCI NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):661-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005851" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; *Apoptosis/drug effects ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Insulin/pharmacology ; Insulin-Like Growth Factor I/*pharmacology ; Morpholines/pharmacology ; Neurons/*cytology/drug effects/enzymology ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Ribosomal Protein S6 Kinases ; *Signal Transduction ; 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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    Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-31
    Description: Nerve growth factor (NGF) induces both differentiation and survival of neurons by binding to the Trk receptor protein tyrosine kinase. Although Ras is required for differentiation, it was not required for NGF-mediated survival of rat pheochromocytoma PC-12 cells in serum-free medium. However, the ability of NGF to prevent apoptosis (programmed cell death) was inhibited by wortmannin or LY294002, two specific inhibitors of phosphatidylinositol (Pl)-3 kinase. Moreover, platelet-derived growth factor (PDGF) prevented apoptosis of PC-12 cells expressing the wild-type PDGF receptor, but not of cells expressing a mutant receptor that failed to activate Pl-3 kinase. Cell survival thus appears to be mediated by a Pl-3 kinase signaling pathway distinct from the pathway that mediates differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yao, R -- Cooper, G M -- R01 CA 18689/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 31;267(5206):2003-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetics, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701324" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Apoptosis/*drug effects ; Cell Differentiation ; Cell Survival/drug effects ; Enzyme Activation ; Nerve Growth Factors/*pharmacology ; PC12 Cells ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Receptors, Platelet-Derived Growth Factor/metabolism ; *Signal Transduction ; ras Proteins/metabolism
    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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    Cellular transforming genes (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-08-27
    Description: Cellular genes potentially capable of inducing oncogenic transformation have been identified by homology to the transforming genes of retroviruses and by the biological activity of cellular DNA's in transfection assays. DNA's of various tumors induce transformation with high efficiencies, indicating that oncogenesis can involve dominant genetic alterations resulting in activation of cellular transforming genes. The identification and characterization of cellular transforming genes and their possible involvement in naturally occurring cancers, is discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooper, G M -- New York, N.Y. -- Science. 1982 Aug 27;217(4562):801-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6285471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Chick Embryo ; DNA/genetics ; DNA Restriction Enzymes ; DNA, Viral/genetics ; Gene Expression Regulation ; *Genes ; Genes, Viral ; Humans ; Mice ; Neoplasms/*genetics ; Oncogene Protein pp60(v-src) ; Rats ; Retroviridae/*genetics ; Transfection ; Viral Proteins/genetics
    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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