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10.1016/j.trecan.2016.05.009 http://scihub22266oqcxt.onion/10.1016/j.trecan.2016.05.009 C5094282!5094282!27819060     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       Trends+Cancer 2016 ; 2 (7): 378-90 Nephropedia Template TP {{tp|p=27819060|t=2016. The Hidden Conundrum of Phosphoinositide Signaling in Cancer |pdf=|usr=}}{{27819060}} gab.com Text The Hidden Conundrum of Phosphoinositide Signaling in Cancer JO: Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=27819060 #FOAvip Phosphoinositide 3-kinase (PI3K) generation of PI(3,4,5)P3 from PI(4,5)P2 and the subsequent activation of Akt and its downstream signaling cascades (e.g. mTORC1) dominates the landscape of phosphoinositide signaling axis in cancer research. However, PI(4,5)P2 is breaking its boundary as merely a substrate for PI3K and phospholipase C (PLC), and is now an established lipid messenger pivotal for different cellular events in cancer. Here, we review the phosphoinositide signaling axis in cancer, giving due weight to PI(4,5)P2 and its generating enzymes, the phosphatidylinositol phosphate (PIP) kinases (PIPKs). We highlighted how PI(4,5)P2 and PIP kinases serve as a proximal node in phosphoinositide signaling axis and how its interaction with cytoskeletal proteins regulates migratory and invasive nexus of metastasizing tumor cells. Twit Text FOAVip The Hidden Conundrum of Phosphoinositide Signaling in Cancer ????Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=27819060 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27819060 #FOAvip English Wikipedia <ref>{{Cite pmid|27819060}}</ref> The Hidden Conundrum of Phosphoinositide Signaling in Cancer #MMPMID27819060 Thapa N; Tan X; Choi S; Lambert PF; Rapraeger AC; Anderson RA Trends Cancer 2016[Jul]; 2 (7): 378-90 PMID27819060show ga Phosphoinositide 3-kinase (PI3K) generation of PI(3,4,5)P3 from PI(4,5)P2 and the subsequent activation of Akt and its downstream signaling cascades (e.g. mTORC1) dominates the landscape of phosphoinositide signaling axis in cancer research. However, PI(4,5)P2 is breaking its boundary as merely a substrate for PI3K and phospholipase C (PLC), and is now an established lipid messenger pivotal for different cellular events in cancer. Here, we review the phosphoinositide signaling axis in cancer, giving due weight to PI(4,5)P2 and its generating enzymes, the phosphatidylinositol phosphate (PIP) kinases (PIPKs). We highlighted how PI(4,5)P2 and PIP kinases serve as a proximal node in phosphoinositide signaling axis and how its interaction with cytoskeletal proteins regulates migratory and invasive nexus of metastasizing tumor cells. äThe Hidden Conundrum of Phosphoinositide Signaling in Cancer (epmc).pdf DeepDyve Pubget Overpricing