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10.1016/j.ccr.2014.04.017 http://scihub22266oqcxt.onion/10.1016/j.ccr.2014.04.017 C4075337!4075337!24882516     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Cell 2014 ; 25 (6): 822-30 Nephropedia Template TP {{tp|p=24882516|t=2014. Mutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP |pdf=|usr=}}{{24882516}} gab.com Text Mutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP JO: Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=24882516 #FOAvip Uveal melanoma (UM) is the most common cancer in adult eyes. Approximately eighty percent of UMs harbor somatic activating mutations in GNAQ or GNA11 (encodes Gq or G11 respectively). Herein, we show in both cell culture and human tumors that cancer-associated Gq/11 mutants activate YAP, a major effector of the Hippo tumor suppressor pathway that is also regulated by G-protein coupled receptor (GPCR) signaling. YAP mediates the oncogenic activity of mutant Gq/11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing Gq/11 mutations. This study reveals an essential role of the Hippo-YAP pathway in Gq/11-induced tumorigenesis and suggests YAP as a potential drug target for UM patients carrying mutations in GNAQ or GNA11. Twit Text FOAVip Mutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP ????Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=24882516 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24882516 #FOAvip English Wikipedia <ref>{{Cite pmid|24882516}}</ref> Mutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP #MMPMID24882516 Yu FX; Luo J; Mo JS; Liu G; Kim YC; Meng Z; Zhao L; Peyman G; Ouyang H; Jiang W; Zhao J; Chen X; Zhang L; Wang CY; Bastian BC; Zhang K; Guan KL Cancer Cell 2014[Jun]; 25 (6): 822-30 PMID24882516show ga Uveal melanoma (UM) is the most common cancer in adult eyes. Approximately eighty percent of UMs harbor somatic activating mutations in GNAQ or GNA11 (encodes Gq or G11 respectively). Herein, we show in both cell culture and human tumors that cancer-associated Gq/11 mutants activate YAP, a major effector of the Hippo tumor suppressor pathway that is also regulated by G-protein coupled receptor (GPCR) signaling. YAP mediates the oncogenic activity of mutant Gq/11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing Gq/11 mutations. This study reveals an essential role of the Hippo-YAP pathway in Gq/11-induced tumorigenesis and suggests YAP as a potential drug target for UM patients carrying mutations in GNAQ or GNA11. äMutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP (epmc).pdf DeepDyve Pubget Overpricing