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10.1038/ncomms15751 http://scihub22266oqcxt.onion/10.1038/ncomms15751 C5472795!5472795 !28604711     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28604711 &cmd=llinks): Failed to open stream: HTTP request failed! 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The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites |pdf=|usr=}}{{28604711 }} gab.com Text The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28604711 #FOAvip Double-strand breaks (DSBs) are repaired through two major pathways, homology-directed recombination (HDR) and non-homologous end joining (NHEJ). While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis). How then is the repair choice made in S/G2 cells? Here we provide evidence demonstrating that APC(Cdh1) plays a critical role in choosing the repair pathways in S/G2 cells. Our results suggest that the default for all DSBs is to recruit 53BP1 and RIF1. BRCA1 is blocked from being recruited to broken ends because its recruitment signal, K63-linked poly-ubiquitin chains on histones, is actively destroyed by the deubiquitinating enzyme USP1. We show that the removal of USP1 depends on APC(Cdh1) and requires Chk1 activation known to be catalysed by ssDNA-RPA-ATR signalling at the ends designated for HDR, linking the status of end processing to RIF1 or BRCA1 recruitment. Twit Text FOAVip The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28604711 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28604711 #FOAvip English Wikipedia <ref>{{Cite pmid|28604711 }}</ref> The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites #MMPMID28604711 Ha K ; Ma C ; Lin H ; Tang L ; Lian Z ; Zhao F ; Li JM ; Zhen B ; Pei H ; Han S ; Malumbres M ; Jin J ; Chen H ; Zhao Y ; Zhu Q ; Zhang P Nat Commun 2017[Jun]; 8 (ä): 15751 PMID28604711 show ga Double-strand breaks (DSBs) are repaired through two major pathways, homology-directed recombination (HDR) and non-homologous end joining (NHEJ). While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis). How then is the repair choice made in S/G2 cells? Here we provide evidence demonstrating that APC(Cdh1) plays a critical role in choosing the repair pathways in S/G2 cells. Our results suggest that the default for all DSBs is to recruit 53BP1 and RIF1. BRCA1 is blocked from being recruited to broken ends because its recruitment signal, K63-linked poly-ubiquitin chains on histones, is actively destroyed by the deubiquitinating enzyme USP1. We show that the removal of USP1 depends on APC(Cdh1) and requires Chk1 activation known to be catalysed by ssDNA-RPA-ATR signalling at the ends designated for HDR, linking the status of end processing to RIF1 or BRCA1 recruitment. |*DNA Damage [MESH] |Anaphase-Promoting Complex-Cyclosome/*physiology [MESH] |Animals [MESH] |Cell Line [MESH] |DNA Breaks, Double-Stranded [MESH] |DNA Repair/*physiology [MESH] |Genomic Instability [MESH] |HEK293 Cells [MESH] |HeLa Cells [MESH] |Humans [MESH] |Mice [MESH] |Models, Genetic [MESH] |Signal Transduction [MESH]The anaphase promoting complex impacts repair choice by protecting ubi(epmc).pdf DeepDyve Pubget Overpricing