Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/ncomms8935 http://scihub22266oqcxt.onion/10.1038/ncomms8935 C5426521!5426521!26228240     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26228240|t=2015. PTEN mediates Notch-dependent stalk cell arrest in angiogenesis |pdf=|usr=}}{{26228240}} gab.com Text PTEN mediates Notch-dependent stalk cell arrest in angiogenesis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26228240 #FOAvip Coordinated activity of VEGF and Notch signals guides the endothelial cell (EC) specification into tip and stalk cells during angiogenesis. Notch activation in stalk cells leads to proliferation arrest via an unknown mechanism. By using gain- and loss-of-function gene-targeting approaches, here we show that PTEN is crucial for blocking stalk cell proliferation downstream of Notch, and this is critical for mouse vessel development. Endothelial deletion of PTEN results in vascular hyperplasia due to a failure to mediate Notch-induced proliferation arrest. Conversely, overexpression of PTEN reduces vascular density and abrogates the increase in EC proliferation induced by Notch blockade. PTEN is a lipid/protein phosphatase that also has nuclear phosphatase-independent functions. We show that both the catalytic and non-catalytic APC/C-Fzr1/Cdh1-mediated activities of PTEN are required for stalk cells' proliferative arrest. These findings define a Notch?PTEN signalling axis as an orchestrator of vessel density and implicate the PTEN-APC/C-Fzr1/Cdh1 hub in angiogenesis. Twit Text FOAVip PTEN mediates Notch-dependent stalk cell arrest in angiogenesis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26228240 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26228240 #FOAvip English Wikipedia <ref>{{Cite pmid|26228240}}</ref> PTEN mediates Notch-dependent stalk cell arrest in angiogenesis #MMPMID26228240 Serra H; Chivite I; Angulo-Urarte A; Soler A; Sutherland JD; Arruabarrena-Aristorena A; Ragab A; Lim R; Malumbres M; Fruttiger M; Potente M; Serrano M; Fabra Ā; Viņals F; Casanovas O; Pandolfi PP; Bigas A; Carracedo A; Gerhardt H; Graupera M Nat Commun 2015[]; 6 (ä): ä PMID26228240show ga Coordinated activity of VEGF and Notch signals guides the endothelial cell (EC) specification into tip and stalk cells during angiogenesis. Notch activation in stalk cells leads to proliferation arrest via an unknown mechanism. By using gain- and loss-of-function gene-targeting approaches, here we show that PTEN is crucial for blocking stalk cell proliferation downstream of Notch, and this is critical for mouse vessel development. Endothelial deletion of PTEN results in vascular hyperplasia due to a failure to mediate Notch-induced proliferation arrest. Conversely, overexpression of PTEN reduces vascular density and abrogates the increase in EC proliferation induced by Notch blockade. PTEN is a lipid/protein phosphatase that also has nuclear phosphatase-independent functions. We show that both the catalytic and non-catalytic APC/C-Fzr1/Cdh1-mediated activities of PTEN are required for stalk cells' proliferative arrest. These findings define a Notch?PTEN signalling axis as an orchestrator of vessel density and implicate the PTEN-APC/C-Fzr1/Cdh1 hub in angiogenesis. äPTEN mediates Notch-dependent stalk cell arrest in angiogenesis (epmc).pdf DeepDyve Pubget Overpricing