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DNA End Resection: Facts and Mechanisms

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 generat...

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Detalles Bibliográficos
Autores principales: Liu, Ting, Huang, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936662/
https://www.ncbi.nlm.nih.gov/pubmed/27240470
http://dx.doi.org/10.1016/j.gpb.2016.05.002
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author Liu, Ting
Huang, Jun
author_facet Liu, Ting
Huang, Jun
author_sort Liu, Ting
collection PubMed
description 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.
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spelling pubmed-49366622016-07-14 DNA End Resection: Facts and Mechanisms Liu, Ting Huang, Jun Genomics Proteomics Bioinformatics Review 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. Elsevier 2016-06 2016-05-27 /pmc/articles/PMC4936662/ /pubmed/27240470 http://dx.doi.org/10.1016/j.gpb.2016.05.002 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Liu, Ting
Huang, Jun
DNA End Resection: Facts and Mechanisms
title DNA End Resection: Facts and Mechanisms
title_full DNA End Resection: Facts and Mechanisms
title_fullStr DNA End Resection: Facts and Mechanisms
title_full_unstemmed DNA End Resection: Facts and Mechanisms
title_short DNA End Resection: Facts and Mechanisms
title_sort dna end resection: facts and mechanisms
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936662/
https://www.ncbi.nlm.nih.gov/pubmed/27240470
http://dx.doi.org/10.1016/j.gpb.2016.05.002
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