title: Nucleotide excision repair in humans.
abstract: The demonstration of DNA damage excision and repair replication by Setlow, Howard-Flanders, Hanawalt and their colleagues in the early 1960s, constituted the discovery of the ubiquitous pathway of nucleotide excision repair (NER). The serial steps in NER are similar in organisms from unicellular bacteria to complex mammals and plants, and involve recognition of lesions, adducts or structures that disrupt the DNA double helix, removal of a short oligonucleotide containing the offending lesion, synthesis of a repair patch copying the opposite undamaged strand, and ligation, to restore the DNA to its original form. The transcription-coupled repair (TCR) subpathway of NER, discovered nearly two decades later, is dedicated to the removal of lesions from the template DNA strands of actively transcribed genes. In this review I will outline the essential factors and complexes involved in NER in humans, and will comment on additional factors and metabolic processes that affect the efficiency of this important process.
authors.affiliation: Department of Biology, Stanford University, Stanford, CA 94305-5020,USA. Electronic address: gspivak@stanford.edu.
authors.forename: Graciela
authors.initials: G
authors.lastname: Spivak
mesh_terms: D002843:Chromatin / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D006801:Humans; D014158:Transcription, Genetic
chemical_list: D002843:Chromatin; D004247:DNA
keywords: DNA repair; Global genome repair; Nucleotide excision repair; Transcription-coupled repair