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Implication of Posttranslational Histone Modifications in Nucleotide Excision Repair
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Int. J. Mol. Sci. 2012, 13(10), 13554-13568; doi:10.3390/ijms131013554

E2F1 and p53 Transcription Factors as Accessory Factors for Nucleotide Excision Repair

Department of Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Science Park, 1801 Park Road 1C, Smithville, TX 78957, USA
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Received: 17 August 2012 / Revised: 10 October 2012 / Accepted: 15 October 2012 / Published: 19 October 2012
(This article belongs to the Special Issue Excising DNA Damage from Chromosomes: Entry Visas and Exit Strategies)
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Abstract

Many of the biochemical details of nucleotide excision repair (NER) have been established using purified proteins and DNA substrates. In cells however, DNA is tightly packaged around histones and other chromatin-associated proteins, which can be an obstacle to efficient repair. Several cooperating mechanisms enhance the efficiency of NER by altering chromatin structure. Interestingly, many of the players involved in modifying chromatin at sites of DNA damage were originally identified as regulators of transcription. These include ATP-dependent chromatin remodelers, histone modifying enzymes and several transcription factors. The p53 and E2F1 transcription factors are well known for their abilities to regulate gene expression in response to DNA damage. This review will highlight the underappreciated, transcription-independent functions of p53 and E2F1 in modifying chromatin structure in response to DNA damage to promote global NER. View Full-Text
Keywords: DNA repair; chromatin; histone acetylation; GCN5; p300 DNA repair; chromatin; histone acetylation; GCN5; p300
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Vélez-Cruz, R.; Johnson, D.G. E2F1 and p53 Transcription Factors as Accessory Factors for Nucleotide Excision Repair. Int. J. Mol. Sci. 2012, 13, 13554-13568.

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