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10.1016/j.cell.2014.06.004 http://scihub22266oqcxt.onion/10.1016/j.cell.2014.06.004 C4110062!4110062!24954536     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24954536&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2014 ; 158 (1): 171-84 Nephropedia Template TP {{tp|p=24954536|t=2014. KRAS and YAP1 converge to regulate EMT and tumor survival |pdf=|usr=}}{{24954536}} gab.com Text KRAS and YAP1 converge to regulate EMT and tumor survival JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=24954536 #FOAvip Cancer cells that express oncogenic alleles of RAS typically require sustained expression of the mutant allele for survival, but the molecular basis of this oncogene dependency remains incompletely understood. To identify genes that can functionally substitute for oncogenic RAS, we systematically expressed 15,294 open reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducible KRAS-specific shRNA. We found 147 genes that promoted survival upon KRAS suppression. In particular, the transcriptional co-activator YAP1 rescued cell viability in KRAS-dependent cells upon suppression of KRAS and was required for KRAS-induced cell transformation. Acquired resistance to Kras suppression in a Kras-driven murine lung cancer model also involved increased YAP1 signaling. KRAS and YAP1 converge on the transcription factor FOS and activate a transcriptional program involved in regulating the epithelial-mesenchymal transition (EMT). Together, these findings implicate transcriptional regulation of EMT by YAP1 as a significant component of oncogenic RAS signaling. Twit Text FOAVip KRAS and YAP1 converge to regulate EMT and tumor survival ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=24954536 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24954536 #FOAvip English Wikipedia <ref>{{Cite pmid|24954536}}</ref> KRAS and YAP1 converge to regulate EMT and tumor survival #MMPMID24954536 Shao DD; Xue W; Krall EB; Bhutkar A; Piccioni F; Wang X; Schinzel AC; Sood S; Rosenbluh J; Kim JW; Zwang Y; Roberts TM; Root DE; Jacks T; Hahn WC Cell 2014[Jul]; 158 (1): 171-84 PMID24954536show ga Cancer cells that express oncogenic alleles of RAS typically require sustained expression of the mutant allele for survival, but the molecular basis of this oncogene dependency remains incompletely understood. To identify genes that can functionally substitute for oncogenic RAS, we systematically expressed 15,294 open reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducible KRAS-specific shRNA. We found 147 genes that promoted survival upon KRAS suppression. In particular, the transcriptional co-activator YAP1 rescued cell viability in KRAS-dependent cells upon suppression of KRAS and was required for KRAS-induced cell transformation. Acquired resistance to Kras suppression in a Kras-driven murine lung cancer model also involved increased YAP1 signaling. KRAS and YAP1 converge on the transcription factor FOS and activate a transcriptional program involved in regulating the epithelial-mesenchymal transition (EMT). Together, these findings implicate transcriptional regulation of EMT by YAP1 as a significant component of oncogenic RAS signaling. äKRAS and YAP1 converge to regulate EMT and tumor survival (epmc).pdf DeepDyve Pubget Overpricing