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10.1016/j.ccell.2016.04.012 http://scihub22266oqcxt.onion/10.1016/j.ccell.2016.04.012 C5124371!5124371!27238081     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Cell 2016 ; 29 (6): 846-58 Nephropedia Template TP {{tp|p=27238081|t=2016. TRIM24 is an oncogenic transcriptional activator in prostate cancer |pdf=|usr=}}{{27238081}} gab.com Text TRIM24 is an oncogenic transcriptional activator in prostate cancer JO: Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=27238081 #FOAvip Androgen receptor (AR) signaling is a key driver of prostate cancer (PC). While androgen-deprivation therapy is transiently effective in advanced disease, tumors often progress to a lethal castration-resistant state (CRPC). We show that recurrent PC-driver mutations in SPOP stabilize the TRIM24 protein, which promotes proliferation under low androgen conditions. TRIM24 augments AR signaling, and AR and TRIM24 co-activated genes are significantly up-regulated in CRPC. Expression of TRIM24 protein increases from primary PC to CRPC, and both TRIM24 protein levels and the AR/TRIM24 gene signature predict disease-recurrence. Analyses in CRPC cells reveal that the TRIM24 bromodomain and the AR-interacting motif are essential to support proliferation. These data provide a rationale for therapeutic TRIM24 targeting in SPOP-mutant and CRPC patients. Twit Text FOAVip TRIM24 is an oncogenic transcriptional activator in prostate cancer ????Cancer Cell http://www.kidney.de/pget.php?&tw=1&pmid=27238081 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27238081 #FOAvip English Wikipedia <ref>{{Cite pmid|27238081}}</ref> TRIM24 is an oncogenic transcriptional activator in prostate cancer #MMPMID27238081 Groner AC; Cato L; de Tribolet-Hardy J; Bernasocchi T; Janouskova H; Melchers D; Houtman R; Cato ACB; Tschopp P; Gu L; Corsinotti A; Zhong Q; Fankhauser C; Fritz C; Poyet C; Wagner U; Guo T; Aebersold R; Garraway LA; Wild PJ; Theurillat JP; Brown M Cancer Cell 2016[Jun]; 29 (6): 846-58 PMID27238081show ga Androgen receptor (AR) signaling is a key driver of prostate cancer (PC). While androgen-deprivation therapy is transiently effective in advanced disease, tumors often progress to a lethal castration-resistant state (CRPC). We show that recurrent PC-driver mutations in SPOP stabilize the TRIM24 protein, which promotes proliferation under low androgen conditions. TRIM24 augments AR signaling, and AR and TRIM24 co-activated genes are significantly up-regulated in CRPC. Expression of TRIM24 protein increases from primary PC to CRPC, and both TRIM24 protein levels and the AR/TRIM24 gene signature predict disease-recurrence. Analyses in CRPC cells reveal that the TRIM24 bromodomain and the AR-interacting motif are essential to support proliferation. These data provide a rationale for therapeutic TRIM24 targeting in SPOP-mutant and CRPC patients. äTRIM24 is an oncogenic transcriptional activator in prostate cancer (epmc).pdf DeepDyve Pubget Overpricing