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10.1615/CritRevOncog.v20.i5-6.110 http://scihub22266oqcxt.onion/10.1615/CritRevOncog.v20.i5-6.110 C5390008!5390008!27279237     free     free     free 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 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Crit+Rev+Oncog 2015 ; 20 (5-6): 391-405 Nephropedia Template TP {{tp|p=27279237|t=2015. Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer |pdf=|usr=}}{{27279237}} gab.com Text Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer JO: Crit Rev Oncog http://www.kidney.de/pget.php?&tw=1&pmid=27279237 #FOAvip Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that regulates multiple cell signaling pathways in both physiological and pathological conditions. Overexpression and activation of FAK is associated with many advanced stage cancers through promoting cancer cell tumorigenicity and progression as well as by regulating the tumor microenvironment. FAK has multiple binding partners through which FAK exerts its functions including RhoGEF, Src family, talin, cortactin, and paxilin. Over the last few years, it has been proposed that a novel group of four transmembrane proteins can interact with FAK and regulate its activity. These include select tetraspanins such as CD151 and CD9 as well as the GAS3 family members epithelial membrane protein-2 (EMP2) and peripheral myelin protein-22 (PMP22). In this review, we discuss the current knowledge of the interaction between FAK and tetraspan proteins in physiological and pathological conditions, with an emphasis on the potential of tetraspan family members as therapeutic targets in cancer. Twit Text FOAVip Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer ????Crit Rev Oncog http://www.kidney.de/pget.php?&tw=1&pmid=27279237 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27279237 #FOAvip English Wikipedia <ref>{{Cite pmid|27279237}}</ref> Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer #MMPMID27279237 Qin Y; Mohandessi S; Gordon L; Wadehra M Crit Rev Oncog 2015[]; 20 (5-6): 391-405 PMID27279237show ga Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that regulates multiple cell signaling pathways in both physiological and pathological conditions. Overexpression and activation of FAK is associated with many advanced stage cancers through promoting cancer cell tumorigenicity and progression as well as by regulating the tumor microenvironment. FAK has multiple binding partners through which FAK exerts its functions including RhoGEF, Src family, talin, cortactin, and paxilin. Over the last few years, it has been proposed that a novel group of four transmembrane proteins can interact with FAK and regulate its activity. These include select tetraspanins such as CD151 and CD9 as well as the GAS3 family members epithelial membrane protein-2 (EMP2) and peripheral myelin protein-22 (PMP22). In this review, we discuss the current knowledge of the interaction between FAK and tetraspan proteins in physiological and pathological conditions, with an emphasis on the potential of tetraspan family members as therapeutic targets in cancer. äRegulation of FAK Activity by Tetraspan Proteins: Potential Clinical I(epmc).pdf DeepDyve Pubget Overpricing