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http://scihub22266oqcxt.onion/ C4741870!4741870!26498689     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 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       Oncotarget 2015 ; 6 (37): 39924-40 Nephropedia Template TP {{tp|p=26498689|t=2015. Key contribution of eIF4H-mediated translational control in tumor promotion |pdf=|usr=}}{{26498689}} gab.com Text Key contribution of eIF4H-mediated translational control in tumor promotion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26498689 #FOAvip Dysregulated expression of translation initiation factors has been associated with carcinogenesis, but underlying mechanisms remains to be fully understood. Here we show that eIF4H (eukaryotic translation initiation factor 4H), an activator of the RNA helicase eIF4A, is overexpressed in lung carcinomas and predictive of response to chemotherapy. In lung cancer cells, depletion of eIF4H enhances sensitization to chemotherapy, decreases cell migration and inhibits tumor growth in vivo, in association with reduced translation of mRNA encoding cell-proliferation (c-Myc, cyclin D1) angiogenic (FGF-2) and anti-apoptotic factors (CIAP-1, BCL-xL). Conversely, each isoform of eIF4H acts as an oncogene in NIH3T3 cells by stimulating transformation, invasion, tumor growth and resistance to drug-induced apoptosis together with increased translation of IRES-containing or structured 5?UTR mRNAs. These results demonstrate that eIF4H plays a crucial role in translational control and can promote cellular transformation by preferentially regulating the translation of potent growth and survival factor mRNAs, indicating that eIF4H is a promising new molecular target for cancer therapy. Twit Text FOAVip Key contribution of eIF4H-mediated translational control in tumor promotion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26498689 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26498689 #FOAvip English Wikipedia <ref>{{Cite pmid|26498689}}</ref> Key contribution of eIF4H-mediated translational control in tumor promotion #MMPMID26498689 Vaysse C; Philippe C; Martineau Y; Quelen C; Hieblot C; Renaud C; Nicaise Y; Desquesnes A; Pannese M; Filleron T; Escourrou G; Lawson M; Rintoul RC; Delisle MB; Pyronnet S; Brousset P; Prats H; Touriol C Oncotarget 2015[Nov]; 6 (37): 39924-40 PMID26498689show ga Dysregulated expression of translation initiation factors has been associated with carcinogenesis, but underlying mechanisms remains to be fully understood. Here we show that eIF4H (eukaryotic translation initiation factor 4H), an activator of the RNA helicase eIF4A, is overexpressed in lung carcinomas and predictive of response to chemotherapy. In lung cancer cells, depletion of eIF4H enhances sensitization to chemotherapy, decreases cell migration and inhibits tumor growth in vivo, in association with reduced translation of mRNA encoding cell-proliferation (c-Myc, cyclin D1) angiogenic (FGF-2) and anti-apoptotic factors (CIAP-1, BCL-xL). Conversely, each isoform of eIF4H acts as an oncogene in NIH3T3 cells by stimulating transformation, invasion, tumor growth and resistance to drug-induced apoptosis together with increased translation of IRES-containing or structured 5?UTR mRNAs. These results demonstrate that eIF4H plays a crucial role in translational control and can promote cellular transformation by preferentially regulating the translation of potent growth and survival factor mRNAs, indicating that eIF4H is a promising new molecular target for cancer therapy. äKey contribution of eIF4H-mediated translational control in tumor prom(epmc).pdf DeepDyve Pubget Overpricing