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Molecular Regulation of UV ‐Induced DNA Repair
Author(s) -
Shah Palak,
He YuYing
Publication year - 2015
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12406
Subject(s) - nucleotide excision repair , xeroderma pigmentosum , dna repair , cockayne syndrome , dna damage , pyrimidine dimer , carcinogenesis , premature aging , biology , base excision repair , genetics , cancer research , dna , cancer
Ultraviolet ( UV ) radiation from sunlight is a major etiologic factor for skin cancer, the most prevalent cancer in the United States, as well as premature skin aging. In particular, UVB radiation causes formation of specific DNA damage photoproducts between pyrimidine bases. These DNA damage photoproducts are repaired by a process called nucleotide excision repair, also known as UV ‐induced DNA repair. When left unrepaired, UVB ‐induced DNA damage leads to accumulation of mutations, predisposing people to carcinogenesis as well as to premature aging. Genetic loss of nucleotide excision repair leads to severe disorders, namely, xeroderma pigmentosum ( XP ), trichothiodystrophy ( TTD ) and Cockayne syndrome ( CS ), which are associated with predisposition to skin carcinogenesis at a young age as well as developmental and neurological conditions. Regulation of nucleotide excision repair is an attractive avenue to preventing or reversing these detrimental consequences of impaired nucleotide excision repair. Here, we review recent studies on molecular mechanisms regulating nucleotide excision repair by extracellular cues and intracellular signaling pathways, with a special focus on the molecular regulation of individual repair factors.