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10.1038/nsmb.2915 http://scihub22266oqcxt.onion/10.1038/nsmb.2915 C4256149!4256149 !25383666     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25383666 &cmd=llinks): Failed to open stream: HTTP request failed! 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Caspase-activated phosphoinositide binding by CNT-1 promotes apoptosis by inhibiting the AKT pathway |pdf=|usr=}}{{25383666 }} gab.com Text Caspase-activated phosphoinositide binding by CNT-1 promotes apoptosis by inhibiting the AKT pathway JO: Nat Struct Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=25383666 #FOAvip Inactivation of cell-survival factors is a crucial step in apoptosis. The phosphoinositide 3-kinase (PI3K)-AKT signaling pathway promotes cell growth, proliferation and survival, and its deregulation causes cancer. How this pathway is suppressed to promote apoptosis is poorly understood. Here we report the identification of a CED-3 caspase substrate in Caenorhabditis elegans, CNT-1, that is cleaved during apoptosis to generate an N-terminal phosphoinositide-binding fragment (tCNT-1). tCNT-1 translocates from the cytoplasm to the plasma membrane and blocks AKT binding to phosphatidylinositol (3,4,5)-trisphosphate, thereby disabling AKT activation and its prosurvival activity. Our findings reveal a new mechanism that negatively regulates AKT cell signaling to promote apoptosis and that may restrict cell growth and proliferation in normal cells. Twit Text FOAVip Caspase-activated phosphoinositide binding by CNT-1 promotes apoptosis by inhibiting the AKT pathway ????Nat Struct Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=25383666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25383666 #FOAvip English Wikipedia <ref>{{Cite pmid|25383666 }}</ref> Caspase-activated phosphoinositide binding by CNT-1 promotes apoptosis by inhibiting the AKT pathway #MMPMID25383666 Nakagawa A ; Sullivan KD ; Xue D Nat Struct Mol Biol 2014[Dec]; 21 (12 ): 1082-90 PMID25383666 show ga Inactivation of cell-survival factors is a crucial step in apoptosis. The phosphoinositide 3-kinase (PI3K)-AKT signaling pathway promotes cell growth, proliferation and survival, and its deregulation causes cancer. How this pathway is suppressed to promote apoptosis is poorly understood. Here we report the identification of a CED-3 caspase substrate in Caenorhabditis elegans, CNT-1, that is cleaved during apoptosis to generate an N-terminal phosphoinositide-binding fragment (tCNT-1). tCNT-1 translocates from the cytoplasm to the plasma membrane and blocks AKT binding to phosphatidylinositol (3,4,5)-trisphosphate, thereby disabling AKT activation and its prosurvival activity. Our findings reveal a new mechanism that negatively regulates AKT cell signaling to promote apoptosis and that may restrict cell growth and proliferation in normal cells. |*Apoptosis [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Binding Sites [MESH] |Caenorhabditis elegans Proteins/chemistry/*metabolism [MESH] |Caenorhabditis elegans/chemistry/*cytology/*metabolism [MESH] |Caspases/metabolism [MESH] |GTPase-Activating Proteins/chemistry/*metabolism [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Phosphatidylinositol Phosphates/metabolism [MESH] |Protein Binding [MESH] |Protein Transport [MESH]Caspase-activated phosphoinositide binding by CNT-1 promotes apoptosis(epmc).pdf DeepDyve Pubget Overpricing