Literature DB >> 16936822

Five repair pathways in one context: chromatin modification during DNA repair.

Yeganeh Ataian1, Jocelyn E Krebs.   

Abstract

The eukaryotic cell is faced with more than 10 000 various kinds of DNA lesions per day. Failure to repair such lesions can lead to mutations, genomic instability, or cell death. Therefore, cells have developed 5 major repair pathways in which different kinds of DNA damage can be detected and repaired: homologous recombination, nonhomologous end joining, nucleotide excision repair, base excision repair, and mismatch repair. However, the efficient repair of DNA damage is complicated by the fact that the genomic DNA is packaged through histone and nonhistone proteins into chromatin, a highly condensed structure that hinders DNA accessibility and its subsequent repair. Therefore, the cellular repair machinery has to circumvent this natural barrier to gain access to the damaged site in a timely manner. Repair of DNA lesions in the context of chromatin occurs with the assistance of ATP-dependent chromatin-remodeling enzymes and histone-modifying enzymes, which allow access of the necessary repair factors to the lesion. Here we review recent studies that elucidate the interplay between chromatin modifiers / remodelers and the major DNA repair pathways.

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Year:  2006        PMID: 16936822     DOI: 10.1139/o06-075

Source DB:  PubMed          Journal:  Biochem Cell Biol        ISSN: 0829-8211            Impact factor:   3.626


  31 in total

1.  Modeling DNA double-strand break repair kinetics as an epiregulated cell-community-wide (epicellcom) response to radiation stress.

Authors:  Bobby R Scott
Journal:  Dose Response       Date:  2011-02-10       Impact factor: 2.658

2.  ATP-dependent chromatin remodeling shapes the DNA replication landscape.

Authors:  Jack A Vincent; Tracey J Kwong; Toshio Tsukiyama
Journal:  Nat Struct Mol Biol       Date:  2008-04-13       Impact factor: 15.369

3.  MBD4-mediated glycosylase activity on a chromatin template is enhanced by acetylation.

Authors:  Toyotaka Ishibashi; Kevin So; Claire G Cupples; Juan Ausió
Journal:  Mol Cell Biol       Date:  2008-06-02       Impact factor: 4.272

Review 4.  DNA Methylation within Transcribed Regions.

Authors:  Taiko K To; Hidetoshi Saze; Tetsuji Kakutani
Journal:  Plant Physiol       Date:  2015-07-04       Impact factor: 8.340

Review 5.  Single nucleotide polymorphisms as susceptibility, prognostic, and therapeutic markers of nonsmall cell lung cancer.

Authors:  Shanbeh Zienolddiny; Vidar Skaug
Journal:  Lung Cancer (Auckl)       Date:  2011-12-29

6.  Embryonic stem cells lacking the epigenetic regulator Cfp1 are hypersensitive to DNA-damaging agents and exhibit decreased Ape1/Ref-1 protein expression and endonuclease activity.

Authors:  Courtney M Tate; Melissa L Fishel; Julianne L Holleran; Merrill J Egorin; David G Skalnik
Journal:  DNA Repair (Amst)       Date:  2009-10-15

7.  Silenced yeast chromatin is maintained by Sir2 in preference to permitting histone acetylations for efficient NER.

Authors:  Agurtzane Irizar; Yachuan Yu; Simon H Reed; Edward J Louis; Raymond Waters
Journal:  Nucleic Acids Res       Date:  2010-04-12       Impact factor: 16.971

Review 8.  Overview for the histone codes for DNA repair.

Authors:  Elizabeth A Williamson; Justin W Wray; Pranshu Bansal; Robert Hromas
Journal:  Prog Mol Biol Transl Sci       Date:  2012       Impact factor: 3.622

9.  Saccharomyces cerevisiae Rad16 mediates ultraviolet-dependent histone H3 acetylation required for efficient global genome nucleotide-excision repair.

Authors:  Yumin Teng; Hairong Liu; Hefin W Gill; Yachuan Yu; Raymond Waters; Simon H Reed
Journal:  EMBO Rep       Date:  2007-11-09       Impact factor: 8.807

10.  Transgenerational stress memory is not a general response in Arabidopsis.

Authors:  Ales Pecinka; Marisa Rosa; Adam Schikora; Marc Berlinger; Heribert Hirt; Christian Luschnig; Ortrun Mittelsten Scheid
Journal:  PLoS One       Date:  2009-04-21       Impact factor: 3.240

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