کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2822407 1161282 2016 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
DNA End Resection: Facts and Mechanisms
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی ژنتیک
پیش نمایش صفحه اول مقاله
DNA End Resection: Facts and Mechanisms
چکیده انگلیسی

DNA double-strand breaks (DSBs), which arise following exposure to a number of endogenous and exogenous agents, can be repaired by either the homologous recombination (HR) or non-homologous end-joining (NHEJ) pathways in eukaryotic cells. A vital step in HR repair is DNA end resection, which generates a long 3′ single-stranded DNA (ssDNA) tail that can invade the homologous DNA strand. The generation of 3′ ssDNA is not only essential for HR repair, but also promotes activation of the ataxia telangiectasia and Rad3-related protein (ATR). Multiple factors, including the MRN/X complex, C-terminal-binding protein interacting protein (CtIP)/Sae2, exonuclease 1 (EXO1), Bloom syndrome protein (BLM)/Sgs1, DNA2 nuclease/helicase, and several chromatin remodelers, cooperate to complete the process of end resection. Here we review the basic machinery involved in DNA end resection in eukaryotic cells.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Genomics, Proteomics & Bioinformatics - Volume 14, Issue 3, June 2016, Pages 126–130
نویسندگان
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