Nucleotide Excision Repair

The function of nucleotide excision repair (NER) is to remove a wide variety of bulky adducts, such as pyrimidine dimers, typically caused by exogenous agents, such as UV light (9,10). The effect of these lesions is to distort the double helix and interfere with replication and transcription. A schematic representation of NER is presented in Figure 1 in Chapter 17. First, the DNA lesion is recognized by a protein complex. Second, unwinding of DNA around the site of damage is accomplished by genetic xeroderma pigmentosum complementation group D (XPD) and XPB helicase activities of the TFIIH transcription factor; the undamaged strand binds replication protein A. Third, endonucleases XPG, ERCC1, and XPF cleave the damaged strand, effectively removing a 24-32 base region containing the damaged DNA. Fourth, the empty gap is filled in by the usual DNA replication machinery, and the ends are sealed by DNA ligase.

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