ArticlePhotochemistry and photobiology
Nucleotide excision repair proteins rapidly accumulate but fail to persist in human XP-E (DDB2 mutant) cells.
Article in Photochemistry and photobiology. 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, 16 citations in OpenAlex.
- Co-infection of HSV-1 amplicons containing theBiochemistry and biophysics reports · 2024Article
- Genomic mutation landscape of skin cancers from DNA repair-deficient xeroderma pigmentosum patients.Nature communications · 2023Article
- Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021Review
- Review
- DNA damage response and repair in perspective: Aedes aegypti, Drosophila melanogaster and Homo sapiens.Parasites & vectors · 2019Review
- Damage sensor role of UV-DDB during base excision repair.Nature structural & molecular biology · 2019Article
- Imaging cellular responses to antigen tagged DNA damage.DNA repair · 2018Review
- Poly(ADP-ribose) polymerase 1 escorts XPC to UV-induced DNA lesions during nucleotide excision repair.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Article
- Orchestral maneuvers at the damaged sites in nucleotide excision repair.Cellular and molecular life sciences : CMLS · 2015Review
- Nucleotide excision repair is reduced in oral epithelial tissues compared with skin.Photochemistry and photobiologyArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The xeroderma pigmentosum (XP-E) DNA damage binding protein (DDB2) is involved in early recognition of global genome DNA damage during DNA nucleotide excision repair (NER). We found that skin fibroblasts from four newly reported XP-E patients with numerous skin cancers and DDB2 mutations had slow repair of 6-4 photoproducts (6-4PP) and markedly reduced repair of cyclobutane pyrimidine dimers (CPD). NER proteins (XPC, XPB, XPG, XPA and XPF) colocalized to CPD and 6-4PP positive regions immediately (<0.1 h) after localized UV irradiation in cells from the XP-E patients and normal controls. While these proteins persist in normal cells, surprisingly, within 0.5 h these repair proteins were no longer detectable at the sites of DNA damage in XP-E cells. Our results indicate that DDB2 is not required for the rapid recruitment of NER proteins to sites of UV photoproducts or for partial repair of 6-4PP but is essential for normal persistence of these proteins for CPD photoproduct removal.
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