Nucleotide Excision Repair in Mammalian Cells*

is found throughout thenatural world in organisms ranging from mycoplasma to mam-mals. In humans, NER is a major defense against the carcino-genic effects of ultraviolet light from the sun. This repair path-way acts with varying efficiencies on a wide variety of DNAalterations and is especially important for bulky, helix-distort-ing lesions. The key event in NER is incision of the damagedstrand on each side of a lesion in DNA, releasing the damage ina fragment that is ;24–32 nucleotides (nt) long in eukaryotes.Nucleotide excision repair defects of various types are found inindividuals with the inherited syndromes xeroderma pigment-osum (XP), Cockayne syndrome (CS), and trichothiodystrophy(1). Individuals with XP are sun-sensitive and generally show agreatly increased incidence of UV-induced skin cancers. Thedisorder has seven genetic complementation groups, desig-nated XP-A through XP-G, and a variant form, XP-V. Therecommended nomenclature uses a hyphen to refer to cells of agiven complementation group (for example XP-A), distinguishingthis from the affected gene

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