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In particular,\n                    <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\n                    radiation causes formation of specific\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    damage photoproducts between pyrimidine bases. These\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    damage photoproducts are repaired by a process called nucleotide excision repair, also known as\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    \u2010induced\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    repair. When left unrepaired,\n                    <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\n                    \u2010induced\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    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 (\n                    <jats:styled-content style=\"fixed-case\">XP<\/jats:styled-content>\n                    ), trichothiodystrophy (\n                    <jats:styled-content style=\"fixed-case\">TTD<\/jats:styled-content>\n                    ) and Cockayne syndrome (\n                    <jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content>\n                    ), 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.\n                  <\/jats:p>","DOI":"10.1111\/php.12406","type":"journal-article","created":{"date-parts":[[2014,12,22]],"date-time":"2014-12-22T10:09:07Z","timestamp":1419242947000},"page":"254-264","source":"Crossref","is-referenced-by-count":75,"title":["Molecular Regulation of\n                    <scp>UV<\/scp>\n                    \u2010Induced\n                    <scp>DNA<\/scp>\n                    Repair"],"prefix":"10.1111","volume":"91","author":[{"given":"Palak","family":"Shah","sequence":"first","affiliation":[{"name":"Department of Medicine Section of Dermatology University of Chicago Chicago IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu\u2010Ying","family":"He","sequence":"additional","affiliation":[{"name":"Department of Medicine Section of Dermatology University of Chicago Chicago IL"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,1,14]]},"reference":[{"key":"e_1_2_15_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-4632.2010.04474.x"},{"key":"e_1_2_15_3_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms140612222"},{"key":"e_1_2_15_4_1","volume-title":"Report on Carcinogens","year":"2011"},{"key":"e_1_2_15_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pbiomolbio.2006.02.023"},{"key":"e_1_2_15_6_1","doi-asserted-by":"publisher","DOI":"10.2741\/cleaver"},{"key":"e_1_2_15_7_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2133.146.s61.2.x"},{"key":"e_1_2_15_8_1","volume-title":"Solar Ultraviolet Radiation: Global Burden of Disease from Solar Ultraviolet Radiation","author":"Lucas R.","year":"2006"},{"key":"e_1_2_15_9_1","volume-title":"Sauer's Manual of Skin Diseases","author":"Hall B. 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