Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.ccell.2015.02.002 http://scihub22266oqcxt.onion/10.1016/j.ccell.2015.02.002 C4357167!4357167!25759020     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Cell 2015 ; 27 (3): 342-53 Nephropedia Template TP {{tp|p=25759020|t=2015. Smoothened variants explain the majority of drug resistance in basal cell carcinoma |pdf=|usr=}}{{25759020}} gab.com Text Smoothened variants explain the majority of drug resistance in basal cell carcinoma JO: Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=25759020 #FOAvip Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms. Here, we identify SMO mutations in 50% (22/44) of resistant BCCs and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand binding pocket mutations defining sites of inhibitor binding and four variants confering constitutive activity and inhibitor resistance, illuminating pivotal residues that ensure receptor autoinhibition. In the presence of a SMO inhibitor, tumor cells containing either class of SMO mutants effectively outcompete cells containing the wild type SMO. Finally, we show that both classes of SMO variants respond to aPKC-?/? or GLI2 inhibitors that operate downstream of SMO, setting the stage for the clinical use of GLI antagonists. Twit Text FOAVip Smoothened variants explain the majority of drug resistance in basal cell carcinoma ????Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=25759020 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25759020 #FOAvip English Wikipedia <ref>{{Cite pmid|25759020}}</ref> Smoothened variants explain the majority of drug resistance in basal cell carcinoma #MMPMID25759020 Atwood SX; Sarin KY; Whitson RJ; Li JR; Kim G; Rezaee M; Ally MS; Kim J; Yao C; Chang ALS; Oro AE; Tang JY Cancer Cell 2015[Mar]; 27 (3): 342-53 PMID25759020show ga Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms. Here, we identify SMO mutations in 50% (22/44) of resistant BCCs and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand binding pocket mutations defining sites of inhibitor binding and four variants confering constitutive activity and inhibitor resistance, illuminating pivotal residues that ensure receptor autoinhibition. In the presence of a SMO inhibitor, tumor cells containing either class of SMO mutants effectively outcompete cells containing the wild type SMO. Finally, we show that both classes of SMO variants respond to aPKC-?/? or GLI2 inhibitors that operate downstream of SMO, setting the stage for the clinical use of GLI antagonists. äSmoothened variants explain the majority of drug resistance in basal c(epmc).pdf DeepDyve Pubget Overpricing