ArticleTranscription
Transcription-coupled repair and apoptosis provide specific protection against transcription-associated mutagenesis by ultraviolet light.
Article in Transcription. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- High cancer-associated mutational burden in normal blood of xeroderma pigmentosum group C, but not groups A, D, or F.Blood neoplasia · 2026Article
- Uniquely high spontaneous mutational load in blood cells of XP-C patients.bioRxiv : the preprint server for biology · 2025Article
- Histone H2Bub dynamics in the 5' region of active genes are tightly linked to the UV-induced transcriptional response.Computational and structural biotechnology journal · 2023Article
- Modeling of autosomal-dominant retinitis pigmentosa in Caenorhabditis elegans uncovers a nexus between global impaired functioning of certain splicing factors and cell type-specific apoptosis.RNA (New York, N.Y.) · 2015Article
- Chromatin structure, transcriptional activity and DNA repair efficiency affect the outcome of chemotherapy in multiple myeloma.British journal of cancer · 2014Article
- Mammalian transcription-coupled excision repair.Cold Spring Harbor perspectives in biology · 2013Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent data reveal that gene transcription affects genome stability in mammalian cells. For example, transcription of DNA that is damaged by the most prevalent exogenous genotoxin, UV light, induces nucleotide substitutions and chromosomal instability, collectively called UV-induced transcription-associated mutations (UV-TAM). An important class of UV-TAM consists of nucleotide transitions that are caused by deamination of cytosine-containing photolesions to uracil, presumably occurring at stalled transcription complexes. Transcription-associated deletions and recombinational events after UV exposure may be triggered by collisions of replication forks with stalled transcription complexes. In this Point-of-View we propose that mammalian cells possess two tailored mechanisms to prevent UV-TAM in dermal stem cells. First, the transcription-coupled nucleotide excision repair (TCR) pathway removes lesions at transcribed DNA strands, forming the primary barrier against the mutagenic consequences of transcription at a damaged template. Second, when TCR is absent or when the capacity of TCR is exceeded, persistently stalled transcription complexes induce apoptosis, averting the generation of mutant cells following replication. We hypothesize that TCR and the apoptotic response in conjunction reduce the risk of skin carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.