{"doi":"10.1111/php.12406","title":"Molecular Regulation of <scp>UV</scp>‐Induced <scp>DNA</scp> Repair","abstract":"<jats:title>Abstract</jats:title><jats:p>Ultraviolet (<jats:styled-content style=\"fixed-case\">UV</jats:styled-content>) 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, <jats:styled-content style=\"fixed-case\">UVB</jats:styled-content> radiation causes formation of specific <jats:styled-content style=\"fixed-case\">DNA</jats:styled-content> damage photoproducts between pyrimidine bases. These <jats:styled-content style=\"fixed-case\">DNA</jats:styled-content> damage photoproducts are repaired by a process called nucleotide excision repair, also known as <jats:styled-content style=\"fixed-case\">UV</jats:styled-content>‐induced <jats:styled-content style=\"fixed-case\">DNA</jats:styled-content> repair. When left unrepaired, <jats:styled-content style=\"fixed-case\">UVB</jats:styled-content>‐induced <jats:styled-content style=\"fixed-case\">DNA</jats:styled-content> 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 (<jats:styled-content style=\"fixed-case\">XP</jats:styled-content>), trichothiodystrophy (<jats:styled-content style=\"fixed-case\">TTD</jats:styled-content>) and Cockayne syndrome (<jats:styled-content style=\"fixed-case\">CS</jats:styled-content>), 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.</jats:p>","journal":"Photochemistry and 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Shah","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":4.290459441148391,"endowment":4.290459441148391,"datacite_reuse_total":6,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"25534312","pmcid":"PMC4355264","openalex_id":"https://openalex.org/W1972931407","authors":[],"funders":[{"funder_name":"American Cancer Society","grant_id":"RSG-13-078-01","title":null},{"funder_name":"NIH","grant_id":"ES016936","title":null},{"funder_name":"NIH","grant_id":"P30 CA014599","title":null},{"funder_name":"NIH","grant_id":"UL1 TR000430","title":null},{"funder_name":"NIEHS NIH HHS","grant_id":"R01 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Repair Mechanisms","Carcinogens and Genotoxicity Assessment","CRISPR and Genetic Engineering","Biology","Medicine","Environmental Science","Aging","Carcinogenesis","Cockayne Syndrome","DNA Repair","DNA Repair Enzymes","DNA-Binding Proteins","Gene Expression Regulation","Humans","RNA Polymerase II","Signal Transduction","Skin Neoplasms","Trichothiodystrophy Syndromes","Ultraviolet Rays","Xeroderma Pigmentosum"],"mesh_terms":["Aging","Cockayne Syndrome","DNA Repair","DNA-Binding Proteins","Gene Expression Regulation","Humans","RNA Polymerase II","Skin Neoplasms","Ultraviolet Rays","Xeroderma Pigmentosum","Signal Transduction","DNA Repair Enzymes","Trichothiodystrophy Syndromes","Carcinogenesis"],"keywords":["Nucleotide excision repair","Xeroderma pigmentosum","DNA repair","Cockayne syndrome","DNA damage","Pyrimidine dimer","Carcinogenesis","Biology","Base excision repair","Premature aging","Cancer research","Genetics","DNA","Cancer"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good 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