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10.1016/j.trecan.2017.01.007 http://scihub22266oqcxt.onion/10.1016/j.trecan.2017.01.007 C5408465!5408465!28462395     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28462395&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       Trends+Cancer 2017 ; 3 (3): 214-24 Nephropedia Template TP {{tp|p=28462395|t=2017. Calmodulin and PI3K Signaling in KRAS Cancers |pdf=|usr=}}{{28462395}} gab.com Text Calmodulin and PI3K Signaling in KRAS Cancers JO: Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28462395 #FOAvip Calmodulin (CaM) uniquely promotes signaling of oncogenic K-Ras; but not N-Ras or H-Ras. How CaM interacts with K-Ras and how this stimulates cell proliferation are among the most challenging questions in KRAS-driven cancers. Earlier data pointed to formation of a ternary complex consisting of K-Ras, PI3K? and CaM. Recent data point to phosphorylated CaM binding to the SH2 domains of the p85 subunit of PI3K? and activating it. Modeling suggests that the high affinity interaction between the phosphorylated CaM tyrosine motif and PI3K?, can promote full PI3K? activation by oncogenic K-Ras. Our up-to-date review discusses CaM?s role in PI3K signaling at the membrane in KRAS-driven cancers. This is significant since it may help development of K-Ras-specific pharmacology. Twit Text FOAVip Calmodulin and PI3K Signaling in KRAS Cancers ????Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28462395 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28462395 #FOAvip English Wikipedia <ref>{{Cite pmid|28462395}}</ref> Calmodulin and PI3K Signaling in KRAS Cancers #MMPMID28462395 Nussinov R; Wang G; Tsai CJ; Jang H; Lu S; Banerjee A; Zhang J; Gaponenko V Trends Cancer 2017[Mar]; 3 (3): 214-24 PMID28462395show ga Calmodulin (CaM) uniquely promotes signaling of oncogenic K-Ras; but not N-Ras or H-Ras. How CaM interacts with K-Ras and how this stimulates cell proliferation are among the most challenging questions in KRAS-driven cancers. Earlier data pointed to formation of a ternary complex consisting of K-Ras, PI3K? and CaM. Recent data point to phosphorylated CaM binding to the SH2 domains of the p85 subunit of PI3K? and activating it. Modeling suggests that the high affinity interaction between the phosphorylated CaM tyrosine motif and PI3K?, can promote full PI3K? activation by oncogenic K-Ras. Our up-to-date review discusses CaM?s role in PI3K signaling at the membrane in KRAS-driven cancers. This is significant since it may help development of K-Ras-specific pharmacology. äCalmodulin and PI3K Signaling in KRAS Cancers (epmc).pdf DeepDyve Pubget Overpricing