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10.1128/MCB.01074-15 http://scihub22266oqcxt.onion/10.1128/MCB.01074-15 C4810475!4810475 !26711268     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26711268 &cmd=llinks): Failed to open stream: HTTP request failed! 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A Switch in Akt Isoforms Is Required for Notch-Induced Snail1 Expression and Protection from Cell Death |pdf=|usr=}}{{26711268 }} gab.com Text A Switch in Akt Isoforms Is Required for Notch-Induced Snail1 Expression and Protection from Cell Death JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26711268 #FOAvip Notch activation in aortic endothelial cells (ECs) takes place at embryonic stages during cardiac valve formation and induces endothelial-to-mesenchymal transition (EndMT). Using aortic ECs, we show here that active Notch expression promotes EndMT, resulting in downregulation of vascular endothelial cadherin (VE-cadherin) and upregulation of mesenchymal genes such as those for fibronectin and Snail1/2. In these cells, transforming growth factor ?1 exacerbates Notch effects by increasing Snail1 and fibronectin activation. When Notch-downstream pathways were analyzed, we detected an increase in glycogen synthase kinase 3? (GSK-3?) phosphorylation and inactivation that facilitates Snail1 nuclear retention and protein stabilization. However, the total activity of Akt was downregulated. The discrepancy between Akt activity and GSK-3? phosphorylation is explained by a Notch-induced switch in the Akt isoforms, whereby Akt1, the predominant isoform expressed in ECs, is decreased and Akt2 transcription is upregulated. Mechanistically, Akt2 induction requires the stimulation of the ?-catenin/TCF4 transcriptional complex, which activates the Akt2 promoter. Active, phosphorylated Akt2 translocates to the nucleus in Notch-expressing cells, resulting in GSK-3? inactivation in this compartment. Akt2, but not Akt1, colocalizes in the nucleus with lamin B in the nuclear envelope. In addition to promoting GSK-3? inactivation, Notch downregulates Forkhead box O1 (FoxO1), another Akt2 nuclear substrate. Moreover, Notch protects ECs from oxidative stress-induced apoptosis through an Akt2- and Snail1-dependent mechanism. Twit Text FOAVip A Switch in Akt Isoforms Is Required for Notch-Induced Snail1 Expression and Protection from Cell Death ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26711268 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26711268 #FOAvip English Wikipedia <ref>{{Cite pmid|26711268 }}</ref> A Switch in Akt Isoforms Is Required for Notch-Induced Snail1 Expression and Protection from Cell Death #MMPMID26711268 Frías A ; Lambies G ; Viñas-Castells R ; Martínez-Guillamon C ; Dave N ; García de Herreros A ; Díaz VM Mol Cell Biol 2015[Dec]; 36 (6 ): 923-40 PMID26711268 show ga Notch activation in aortic endothelial cells (ECs) takes place at embryonic stages during cardiac valve formation and induces endothelial-to-mesenchymal transition (EndMT). Using aortic ECs, we show here that active Notch expression promotes EndMT, resulting in downregulation of vascular endothelial cadherin (VE-cadherin) and upregulation of mesenchymal genes such as those for fibronectin and Snail1/2. In these cells, transforming growth factor ?1 exacerbates Notch effects by increasing Snail1 and fibronectin activation. When Notch-downstream pathways were analyzed, we detected an increase in glycogen synthase kinase 3? (GSK-3?) phosphorylation and inactivation that facilitates Snail1 nuclear retention and protein stabilization. However, the total activity of Akt was downregulated. The discrepancy between Akt activity and GSK-3? phosphorylation is explained by a Notch-induced switch in the Akt isoforms, whereby Akt1, the predominant isoform expressed in ECs, is decreased and Akt2 transcription is upregulated. Mechanistically, Akt2 induction requires the stimulation of the ?-catenin/TCF4 transcriptional complex, which activates the Akt2 promoter. Active, phosphorylated Akt2 translocates to the nucleus in Notch-expressing cells, resulting in GSK-3? inactivation in this compartment. Akt2, but not Akt1, colocalizes in the nucleus with lamin B in the nuclear envelope. In addition to promoting GSK-3? inactivation, Notch downregulates Forkhead box O1 (FoxO1), another Akt2 nuclear substrate. Moreover, Notch protects ECs from oxidative stress-induced apoptosis through an Akt2- and Snail1-dependent mechanism. |*Cell Death [MESH] |Animals [MESH] |Aorta/cytology [MESH] |Cell Line [MESH] |Endothelial Cells/cytology/metabolism [MESH] |Epithelial-Mesenchymal Transition [MESH] |Gene Expression Regulation [MESH] |Glycogen Synthase Kinase 3 beta [MESH] |Glycogen Synthase Kinase 3/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Mice [MESH] |Oxidative Stress [MESH] |Protein Isoforms/analysis/genetics/metabolism [MESH] |Protein Stability [MESH] |Proto-Oncogene Proteins c-akt/analysis/genetics/*metabolism [MESH] |Receptors, Notch/*metabolism [MESH] |Snail Family Transcription Factors [MESH] |Swine [MESH] |Transcription Factors/analysis/*genetics/metabolism [MESH] |Up-Regulation [MESH]A Switch in Akt Isoforms Is Required for Notch-Induced Snail1 Expressi(epmc).pdf DeepDyve Pubget Overpricing