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10.1016/j.ceb.2017.01.003 http://scihub22266oqcxt.onion/10.1016/j.ceb.2017.01.003 C5482783!5482783 !28213315     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28213315 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28213315 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Cell+Biol 2017 ; 45 (ä): 24-30 Nephropedia Template TP {{tp|p=28213315 |t=2017. Focal adhesion kinase signaling in unexpected places |pdf=|usr=}}{{28213315 }} gab.com Text Focal adhesion kinase signaling in unexpected places JO: Curr Opin Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28213315 #FOAvip Focal adhesion kinase (FAK) is a cytoplasmic protein-tyrosine kinase first identified at extracellular matrix and integrin receptor cell adhesion sites and is a key regulator of cell movement. FAK is activated by a variety of stimuli. Herein, we discuss advances in conformational-associated FAK activation and dimerization mechanisms. Additionally, new roles have emerged for FAK signaling at cell adhesions, adherens junctions, endosomes, and the nucleus. In light of these new findings, we review how FAK activation at these sites is connected to the regulation of integrin recycling-activation, vascular permeability, cell survival, and transcriptional regulation, respectively. Studies uncovering FAK signaling connections in unexpected places within cells have yielded important new regulatory insights in cell biology. Twit Text FOAVip Focal adhesion kinase signaling in unexpected places ????Curr Opin Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28213315 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28213315 #FOAvip English Wikipedia <ref>{{Cite pmid|28213315 }}</ref> Focal adhesion kinase signaling in unexpected places #MMPMID28213315 Kleinschmidt EG ; Schlaepfer DD Curr Opin Cell Biol 2017[Apr]; 45 (ä): 24-30 PMID28213315 show ga Focal adhesion kinase (FAK) is a cytoplasmic protein-tyrosine kinase first identified at extracellular matrix and integrin receptor cell adhesion sites and is a key regulator of cell movement. FAK is activated by a variety of stimuli. Herein, we discuss advances in conformational-associated FAK activation and dimerization mechanisms. Additionally, new roles have emerged for FAK signaling at cell adhesions, adherens junctions, endosomes, and the nucleus. In light of these new findings, we review how FAK activation at these sites is connected to the regulation of integrin recycling-activation, vascular permeability, cell survival, and transcriptional regulation, respectively. Studies uncovering FAK signaling connections in unexpected places within cells have yielded important new regulatory insights in cell biology. |*Signal Transduction [MESH] |Adherens Junctions/*metabolism [MESH] |Animals [MESH] |Binding Sites [MESH] |Cell Adhesion [MESH] |Cell Movement [MESH] |Endosomes/metabolism [MESH] |Enzyme Activation [MESH] |Extracellular Matrix/metabolism [MESH] |Focal Adhesion Protein-Tyrosine Kinases/chemistry/*metabolism [MESH] |Humans [MESH] |Integrins/metabolism [MESH]Focal adhesion kinase signaling in unexpected places (epmc).pdf DeepDyve Pubget Overpricing