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10.1080/15384101.2018.1456296 http://scihub22266oqcxt.onion/10.1080/15384101.2018.1456296 C6056224!6056224!29683380     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Cycle 2018 ; 17 (7): 833-43 Nephropedia Template TP {{tp|p=29683380|t=2018. Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis |pdf=|usr=}}{{29683380}} gab.com Text Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis JO: Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=29683380 #FOAvip Mutagenesis is a hallmark and enabling characteristic of cancer cells. The E3 ubiquitin ligase RAD18 and its downstream effectors, the ?Y-family? Trans-Lesion Synthesis (TLS) DNA polymerases, confer DNA damage tolerance at the expense of DNA replication fidelity. Thus, RAD18 and TLS polymerases are attractive candidate mediators of mutagenesis and carcinogenesis. The skin cancer-propensity disorder xeroderma pigmentosum-variant (XPV) is caused by defects in the Y-family DNA polymerase Pol eta (Pol?). However it is unknown whether TLS dysfunction contributes more generally to other human cancers. Recent analyses of cancer genomes suggest that TLS polymerases generate many of the mutational signatures present in diverse cancers. Moreover biochemical studies suggest that the TLS pathway is often reprogrammed in cancer cells and that TLS facilitates tolerance of oncogene-induced DNA damage. Here we review recent evidence supporting widespread participation of RAD18 and the Y-family DNA polymerases in the different phases of multi-step carcinogenesis. Twit Text FOAVip Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis ????Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=29683380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29683380 #FOAvip English Wikipedia <ref>{{Cite pmid|29683380}}</ref> Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis #MMPMID29683380 Yang Y; Gao Y; Zlatanou A; Tateishi S; Yurchenko V; Rogozin IB; Vaziri C Cell Cycle 2018[]; 17 (7): 833-43 PMID29683380show ga Mutagenesis is a hallmark and enabling characteristic of cancer cells. The E3 ubiquitin ligase RAD18 and its downstream effectors, the ?Y-family? Trans-Lesion Synthesis (TLS) DNA polymerases, confer DNA damage tolerance at the expense of DNA replication fidelity. Thus, RAD18 and TLS polymerases are attractive candidate mediators of mutagenesis and carcinogenesis. The skin cancer-propensity disorder xeroderma pigmentosum-variant (XPV) is caused by defects in the Y-family DNA polymerase Pol eta (Pol?). However it is unknown whether TLS dysfunction contributes more generally to other human cancers. Recent analyses of cancer genomes suggest that TLS polymerases generate many of the mutational signatures present in diverse cancers. Moreover biochemical studies suggest that the TLS pathway is often reprogrammed in cancer cells and that TLS facilitates tolerance of oncogene-induced DNA damage. Here we review recent evidence supporting widespread participation of RAD18 and the Y-family DNA polymerases in the different phases of multi-step carcinogenesis. äDiverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis (epmc).pdf DeepDyve Pubget Overpricing