ArticleNucleic acids research2023
Nucleotide excision repair in Human cell lines lacking both XPC and CSB proteins.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Effect of xeroderma pigmentosum group C on the characteristics and regulatory mechanisms of lung cancer stem cells.International journal of oncology · 2026Article
- Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025Review
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
- XPD stalled on cross-linked DNA provides insight into damage verification.Nature structural & molecular biology · 2024Article
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.Genetics · 2024Article
- Genome-wide analysis of transcription-coupled repair reveals novel transcription events in Caenorhabditis elegans.PLoS genetics · 2024Article
- Genome-wide analysis of transcription-coupled repair reveals novel transcription events inbioRxiv : the preprint server for biology · 2024Article
- Cross-species investigation into the requirement of XPA for nucleotide excision repair.Nucleic acids research · 2024Article
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nucleotide excision repair removes UV-induced DNA damage through two distinct sub-pathways, global repair and transcription-coupled repair (TCR). Numerous studies have shown that in human and other mammalian cell lines that the XPC protein is required for repair of DNA damage from nontranscribed DNA via global repair and the CSB protein is required for repair of lesions from transcribed DNA via TCR. Therefore, it is generally assumed that abrogating both sub-pathways with an XPC-/-/CSB-/- double mutant would eliminate all nucleotide excision repair. Here we describe the construction of three different XPC-/-/CSB-/- human cell lines that, contrary to expectations, perform TCR. The XPC and CSB genes were mutated in cell lines derived from Xeroderma Pigmentosum patients as well as from normal human fibroblasts and repair was analyzed at the whole genome level using the very sensitive XR-seq method. As predicted, XPC-/- cells exhibited only TCR and CSB-/- cells exhibited only global repair. However, the XPC-/-/CSB-/- double mutant cell lines, although having greatly reduced repair, exhibited TCR. Mutating the CSA gene to generate a triple mutant XPC-/-/CSB-/-/CSA-/- cell line eliminated all residual TCR activity. Together, these findings provide new insights into the mechanistic features of mammalian nucleotide excision repair.
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