Int. J. Mol. Sci. 2012, 13(10), 13554-13568; doi:10.3390/ijms131013554
Review

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

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Received: 17 August 2012; in revised form: 10 October 2012 / Accepted: 15 October 2012 / Published: 19 October 2012
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Keywords: DNA repair; chromatin; histone acetylation; GCN5; p300
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MDPI and ACS Style

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.

AMA Style

Vélez-Cruz R, Johnson DG. E2F1 and p53 Transcription Factors as Accessory Factors for Nucleotide Excision Repair. International Journal of Molecular Sciences. 2012; 13(10):13554-13568.

Chicago/Turabian Style

Vélez-Cruz, Renier; Johnson, David G. 2012. "E2F1 and p53 Transcription Factors as Accessory Factors for Nucleotide Excision Repair." Int. J. Mol. Sci. 13, no. 10: 13554-13568.

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