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10.1101/gad.288282.116 http://scihub22266oqcxt.onion/10.1101/gad.288282.116 C5159665!5159665 !27940962     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27940962 &cmd=llinks): Failed to open stream: HTTP request failed! 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RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1 |pdf=|usr=}}{{27940962 }} gab.com Text RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1 JO: Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=27940962 #FOAvip The retinoblastoma (RB) tumor suppressor is recognized as a master regulator that controls entry into the S phase of the cell cycle. Its loss leads to uncontrolled cell proliferation and is a hallmark of cancer. RB works by binding to members of the E2F family of transcription factors and recruiting chromatin modifiers to the promoters of E2F target genes. Here we show that RB also localizes to DNA double-strand breaks (DSBs) dependent on E2F1 and ATM kinase activity and promotes DSB repair through homologous recombination (HR), and its loss results in genome instability. RB is necessary for the recruitment of the BRG1 ATPase to DSBs, which stimulates DNA end resection and HR. A knock-in mutation of the ATM phosphorylation site on E2F1 (S29A) prevents the interaction between E2F1 and TopBP1 and recruitment of RB, E2F1, and BRG1 to DSBs. This knock-in mutation also impairs DNA repair, increases genomic instability, and renders mice hypersensitive to IR. Importantly, depletion of RB in osteosarcoma and breast cancer cell lines results in sensitivity to DNA-damaging drugs, which is further exacerbated by poly-ADP ribose polymerase (PARP) inhibitors. We uncovered a novel, nontranscriptional function for RB in HR, which could contribute to genome instability associated with RB loss. Twit Text FOAVip RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1 ????Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=27940962 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27940962 #FOAvip English Wikipedia <ref>{{Cite pmid|27940962 }}</ref> RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1 #MMPMID27940962 Vélez-Cruz R ; Manickavinayaham S ; Biswas AK ; Clary RW ; Premkumar T ; Cole F ; Johnson DG Genes Dev 2016[Nov]; 30 (22 ): 2500-2512 PMID27940962 show ga The retinoblastoma (RB) tumor suppressor is recognized as a master regulator that controls entry into the S phase of the cell cycle. Its loss leads to uncontrolled cell proliferation and is a hallmark of cancer. RB works by binding to members of the E2F family of transcription factors and recruiting chromatin modifiers to the promoters of E2F target genes. Here we show that RB also localizes to DNA double-strand breaks (DSBs) dependent on E2F1 and ATM kinase activity and promotes DSB repair through homologous recombination (HR), and its loss results in genome instability. RB is necessary for the recruitment of the BRG1 ATPase to DSBs, which stimulates DNA end resection and HR. A knock-in mutation of the ATM phosphorylation site on E2F1 (S29A) prevents the interaction between E2F1 and TopBP1 and recruitment of RB, E2F1, and BRG1 to DSBs. This knock-in mutation also impairs DNA repair, increases genomic instability, and renders mice hypersensitive to IR. Importantly, depletion of RB in osteosarcoma and breast cancer cell lines results in sensitivity to DNA-damaging drugs, which is further exacerbated by poly-ADP ribose polymerase (PARP) inhibitors. We uncovered a novel, nontranscriptional function for RB in HR, which could contribute to genome instability associated with RB loss. |*DNA Breaks, Double-Stranded/drug effects/radiation effects [MESH] |Animals [MESH] |Cell Line [MESH] |Cell Line, Tumor [MESH] |DNA Helicases/genetics/*metabolism [MESH] |DNA Repair/genetics [MESH] |E2F1 Transcription Factor/genetics/metabolism [MESH] |Gamma Rays [MESH] |Gene Knock-In Techniques [MESH] |Genomic Instability/genetics [MESH] |Homologous Recombination/*genetics [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Mutagens/pharmacology [MESH] |Mutation [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |Poly(ADP-ribose) Polymerase Inhibitors/pharmacology [MESH] |Protein Transport/genetics [MESH] |Retinoblastoma Protein/genetics/*metabolism [MESH] |Transcription Factors/genetics/*metabolism [MESH]RB localizes to DNA double-strand breaks and promotes DNA end resectio(epmc).pdf DeepDyve Pubget Overpricing