ArticleProceedings of the National Academy of Sciences of the United States of America2003
UV wavelength-dependent regulation of transcription-coupled nucleotide excision repair in p53-deficient human cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin.Oxidative medicine and cellular longevity · 2016Trial
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- A majority of human melanoma cell lines exhibits an S phase-specific defect in excision of UV-induced DNA photoproducts.PloS one · 2014Article
- Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The role of altered nucleotide excision repair and UVB-induced DNA damage in melanomagenesis.International journal of molecular sciences · 2013Review
- Wavelength dependence of ultraviolet radiation-induced DNA damage as determined by laser irradiation suggests that cyclobutane pyrimidine dimers are the principal DNA lesions produced by terrestrial sunlight.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- UV-induced association of the CSB remodeling protein with chromatin requires ATP-dependent relief of N-terminal autorepression.Molecular cell · 2010Article
- ATR kinase is required for global genomic nucleotide excision repair exclusively during S phase in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Human glyceraldehyde-3-phosphate dehydrogenase plays a direct role in reactivating oxidized forms of the DNA repair enzyme APE1.The Journal of biological chemistry · 2008Article
- Rapid repair of UVA-induced oxidized purines and persistence of UVB-induced dipyrimidine lesions determine the mutagenicity of sunlight in mouse cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008Article
- The novel PIAS-like protein hZimp10 is a transcriptional co-activator of the p53 tumor suppressor.Nucleic acids research · 2007Article
- Structure, function and regulation of CSB: a multi-talented gymnast.Mechanisms of ageing and developmentReview
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide excision repair (NER) prevents skin cancer by eliminating highly genotoxic cyclobutane pyrimidine dimers (CPDs) induced in DNA by the UVB component of sunlight. NER consists of two distinct but overlapping subpathways, i.e., global NER, which removes CPD from the genome overall, and transcription-coupled NER (TCNER), which removes CPD uniquely from the transcribed strand of active genes. Previous investigations have clearly established that the p53 tumor suppressor plays a crucial role in the NER process. Here we used the ligation-mediated PCR technique to demonstrate, at nucleotide resolution along two chromosomal genes in human cells, that the requirement for functional p53 in TCNER, but not in global NER, depends on incident UV wavelength. Indeed, relative to an isogenic p53 wild-type counterpart, p53-deficient human lymphoblastoid strains were shown to remove CPD significantly less efficiently along both the transcribed and nontranscribed strands of the c-jun and hprt loci after exposure to polychromatic UVB (290-320 nm). However, in contrast, after irradiation with 254-nm UV, p53 deficiency engendered less efficient CPD repair only along the nontranscribed strands of these target genes. The revelation of this intriguing wavelength-dependent phenomenon reconciles an apparent conflict between previous studies which used either UVB or 254-nm UV to claim, respectively, that p53 is required for, or plays no role whatsoever in, TCNER of CPD. Furthermore, our finding highlights a major caveat in experimental photobiology by providing a prominent example where the extensively used "nonsolar" model mutagen 254-nm UV does not accurately replicate the effects of environmentally relevant UVB.
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