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10.1016/j.cub.2017.06.020 http://scihub22266oqcxt.onion/10.1016/j.cub.2017.06.020 C5667920!5667920!28712573     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28712573&cmd=llinks): Failed to open stream: HTTP request failed! 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VE-cadherin phosphorylation regulates endothelial fluid shear stress responses through the polarity protein LGN |pdf=|usr=}}{{28712573}} gab.com Text VE-cadherin phosphorylation regulates endothelial fluid shear stress responses through the polarity protein LGN JO: Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=28712573 #FOAvip Fluid shear stress due to blood flow on the vascular endothelium regulates blood vessel development, remodeling, physiology and pathology [1, 2]. A complex consisting of PECAM-1, VE-cadherin and vascular endothelial growth factor receptors (VEGFRs) that resides at endothelial cell-cell junctions transduces signals important for flow-dependent vasodilation, blood vessel remodeling and atherosclerosis. PECAM-1 transduce forces to activate src family kinases (SFKs), which phosphorylate and transactivate VEGFRs [3-5]. By contrast, VE-cadherin functions as an adapter that interacts with VEGFRs through their respective cytoplasmic domains and promotes VEGFR activation in flow [6]. Indeed, shear stress triggers rapid increases in force across PECAM-1 but decreases the force across VE-cadherin, in close association with downstream signaling [5]. Interestingly, VE-cadherin cytoplasmic tyrosine Y658 can be phosphorylated by SFKs [7], which is maximally induced by low shear stress in vitro and in vivo [8]. These considerations prompted us to address the involvement of VE-cadherin cytoplasmic tyrosines in flow sensing. We found that phosphorylation of a small pool of VE-cadherin on Y658 is essential for flow sensing through the junctional complex. Y658 phosphorylation induces dissociation of p120ctn, which allows binding of the polarity protein LGN. LGN is then required for multiple flow responses in vitro and in vivo, including activation of inflammatory signaling at regions of disturbed flow, and flow-dependent vascular remodeling. Thus, endothelial flow mechanotransduction through the junctional complex is mediated by a specific pool of VE-cadherin that is phosphorylated on Y658 and bound to LGN. Twit Text FOAVip VE-cadherin phosphorylation regulates endothelial fluid shear stress responses through the polarity protein LGN ????Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=28712573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28712573 #FOAvip English Wikipedia <ref>{{Cite pmid|28712573}}</ref> VE-cadherin phosphorylation regulates endothelial fluid shear stress responses through the polarity protein LGN #MMPMID28712573 Conway DE; Coon BG; Budatha M; Arsenovic PT; Orsenigo F; Wessel F; Zhang J; Zhuang ZW; Dejana E; Vestweber D; Schwartz MA Curr Biol 2017[Jul]; 27 (14): 2219-2225.e5 PMID28712573show ga Fluid shear stress due to blood flow on the vascular endothelium regulates blood vessel development, remodeling, physiology and pathology [1, 2]. A complex consisting of PECAM-1, VE-cadherin and vascular endothelial growth factor receptors (VEGFRs) that resides at endothelial cell-cell junctions transduces signals important for flow-dependent vasodilation, blood vessel remodeling and atherosclerosis. PECAM-1 transduce forces to activate src family kinases (SFKs), which phosphorylate and transactivate VEGFRs [3-5]. By contrast, VE-cadherin functions as an adapter that interacts with VEGFRs through their respective cytoplasmic domains and promotes VEGFR activation in flow [6]. Indeed, shear stress triggers rapid increases in force across PECAM-1 but decreases the force across VE-cadherin, in close association with downstream signaling [5]. Interestingly, VE-cadherin cytoplasmic tyrosine Y658 can be phosphorylated by SFKs [7], which is maximally induced by low shear stress in vitro and in vivo [8]. These considerations prompted us to address the involvement of VE-cadherin cytoplasmic tyrosines in flow sensing. We found that phosphorylation of a small pool of VE-cadherin on Y658 is essential for flow sensing through the junctional complex. Y658 phosphorylation induces dissociation of p120ctn, which allows binding of the polarity protein LGN. LGN is then required for multiple flow responses in vitro and in vivo, including activation of inflammatory signaling at regions of disturbed flow, and flow-dependent vascular remodeling. Thus, endothelial flow mechanotransduction through the junctional complex is mediated by a specific pool of VE-cadherin that is phosphorylated on Y658 and bound to LGN. �VE-cadherin phosphorylation regulates endothelial fluid shear stress r(epmc).pdf DeepDyve Pubget Overpricing