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

被引:13
|
作者
Velez-Cruz, Renier [1 ]
Johnson, David G. [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Mol Carcinogenesis, Smithville, TX 78957 USA
来源
基金
美国国家卫生研究院;
关键词
DNA repair; chromatin; histone acetylation; GCN5; p300; DNA-DAMAGE RESPONSE; RNA-POLYMERASE-II; ATM-DEPENDENT PHOSPHORYLATION; STRAND BREAK REPAIR; TUMOR-SUPPRESSOR; XERODERMA-PIGMENTOSUM; COCKAYNE-SYNDROME; HUMAN-CELLS; UV-IRRADIATION; IN-VIVO;
D O I
10.3390/ijms131013554
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:13554 / 13568
页数:15
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