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10.1091/mbc.E15-06-0338 http://scihub22266oqcxt.onion/10.1091/mbc.E15-06-0338 C4551318!4551318 !26157164     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26157164 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26157164 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Biol+Cell 2015 ; 26 (17 ): 3047-60 Nephropedia Template TP {{tp|p=26157164 |t=2015. Actin remodeling by Nck regulates endothelial lumen formation |pdf=|usr=}}{{26157164 }} gab.com Text Actin remodeling by Nck regulates endothelial lumen formation JO: Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=26157164 #FOAvip Multiple angiogenic cues modulate phosphotyrosine signaling to promote vasculogenesis and angiogenesis. Despite its functional and clinical importance, how vascular cells integrate phosphotyrosine-dependent signaling to elicit cytoskeletal changes required for endothelial morphogenesis remains poorly understood. The family of Nck adaptors couples phosphotyrosine signals with actin dynamics and therefore is well positioned to orchestrate cellular processes required in vascular formation and remodeling. Culture of endothelial cells in three-dimensional collagen matrices in the presence of VEGF stimulation was combined with molecular genetics, optical imaging, and biochemistry to show that Nck-dependent actin remodeling promotes endothelial cell elongation and proper organization of VE-cadherin intercellular junctions. Major morphogenetic defects caused by abrogation of Nck signaling included loss of endothelial apical-basal polarity and impaired lumenization. Time-lapse imaging using a Förster resonance energy transfer biosensor, immunostaining with phospho-specific antibodies, and GST pull-down assays showed that Nck determines spatiotemporal patterns of Cdc42/aPKC activation during endothelial morphogenesis. Our results demonstrate that Nck acts as an important hub integrating angiogenic cues with cytoskeletal changes that enable endothelial apical-basal polarization and lumen formation. These findings point to Nck as an emergent target for effective antiangiogenic therapy. Twit Text FOAVip Actin remodeling by Nck regulates endothelial lumen formation ????Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=26157164 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26157164 #FOAvip English Wikipedia <ref>{{Cite pmid|26157164 }}</ref> Actin remodeling by Nck regulates endothelial lumen formation #MMPMID26157164 Chaki SP ; Barhoumi R ; Rivera GM Mol Biol Cell 2015[Sep]; 26 (17 ): 3047-60 PMID26157164 show ga Multiple angiogenic cues modulate phosphotyrosine signaling to promote vasculogenesis and angiogenesis. Despite its functional and clinical importance, how vascular cells integrate phosphotyrosine-dependent signaling to elicit cytoskeletal changes required for endothelial morphogenesis remains poorly understood. The family of Nck adaptors couples phosphotyrosine signals with actin dynamics and therefore is well positioned to orchestrate cellular processes required in vascular formation and remodeling. Culture of endothelial cells in three-dimensional collagen matrices in the presence of VEGF stimulation was combined with molecular genetics, optical imaging, and biochemistry to show that Nck-dependent actin remodeling promotes endothelial cell elongation and proper organization of VE-cadherin intercellular junctions. Major morphogenetic defects caused by abrogation of Nck signaling included loss of endothelial apical-basal polarity and impaired lumenization. Time-lapse imaging using a Förster resonance energy transfer biosensor, immunostaining with phospho-specific antibodies, and GST pull-down assays showed that Nck determines spatiotemporal patterns of Cdc42/aPKC activation during endothelial morphogenesis. Our results demonstrate that Nck acts as an important hub integrating angiogenic cues with cytoskeletal changes that enable endothelial apical-basal polarization and lumen formation. These findings point to Nck as an emergent target for effective antiangiogenic therapy. |Actin Cytoskeleton/genetics/*metabolism [MESH] |Adaptor Proteins, Signal Transducing/genetics/*metabolism [MESH] |Cell Line [MESH] |Endothelial Cells/*cytology/*metabolism [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |Intercellular Junctions/metabolism [MESH] |Oncogene Proteins/genetics/*metabolism [MESH] |Phosphotyrosine/metabolism [MESH] |Signal Transduction [MESH] |Spatio-Temporal Analysis [MESH]Actin remodeling by Nck regulates endothelial lumen formation (epmc).pdf DeepDyve Pubget Overpricing