Article Abstract:
DNA polymerase eta has been found to be defective in various ways in xeroderma pigmentosum variant cells. The polymerase carries out translesion synthesis past ultraviolet (UV) photoproducts. Study shows that pol(eta) is localized uniformly in the nucleus for the most part after UV irradiation of human fibroblasts, but is associated with replication foci in S phase. Relocalization of pol(eta) is required for it to function. Sequences needed for relocalization have been found.
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Article Abstract:
The xeroderma pigmentosum group D (XPD) gene is discussed in this review article. Most people with xeroderma pigmentosum are not able to repair damage in DNA from ultraviolet (UV) light from the sun. Those with hereditary nonpolyposis colon carcinoma do not repair mismatched bases normally. Trichothiodystrophy, involving low-sulfur brittle hair with lack of cysteine-rich matrix proteins, Cockayne syndrome with XP, and the role of XPD in the TFIIH complex, TFIIH being a basal transcription factor, are covered.
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Article Abstract:
Damage recognition for nucleotide excision repair (NER) seems to require at least two steps. The multistep mechanism found may give a molecular basis for ensuring the high level of damage discrimination needed for global genomic NER. A detailed analysis of the binding specificity of the XPC-HR23B complex has been described with various DNA substrates used, each with one defined lesion. The XPC-HR23B complex, a mammalian NER factor, can bind specifically to certain DNA lesions and start the cell-free repair reaction. Additional factors and steps are likely neded for recognition of some kinds of lesions. Genetic aspects of xeroderma pigmentosum are discussed.
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