ArticleProceedings of the National Academy of Sciences of the United States of America2013
Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- PAF1C restores transcription after DNA damage independently of promoting histone mark deposition.EMBO reports · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Cockayne syndrome B protein is implicated in transcription and associated chromatin dynamics in homeostatic and genotoxic conditions.Aging cell · 2025Article
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Clinical and molecular overlap between nucleotide excision repair (NER) disorders andFrontiers in neuroscience · 2025Article
- STK19 facilitates the clearance of lesion-stalled RNAPII during transcription-coupled DNA repair.Cell · 2024Article
- Article
- Next-generation sequencing through multi-gene panel testing for the diagnosis of a Chinese patient with atypical Cockayne syndrome.Molecular genetics & genomic medicine · 2023Article
- Article
- Enhanced frequency of transcription pre-initiation complexes assembly after exposure to UV irradiation results in increased repair activity and reduced probabilities for mutagenesis.Nucleic acids research · 2023Article
- Non-viral gene therapy using RNA interference with PDGFR-α mediated epithelial-mesenchymal transformation for proliferative vitreoretinopathy.Materials today. Bio · 2023Article
- Active mRNA degradation by EXD2 nuclease elicits recovery of transcription after genotoxic stress.Nature communications · 2023Article
- Microglial activating transcription factor 3 upregulation: An indirect target to attenuate inflammation in the nervous system.Frontiers in molecular neuroscience · 2023Article
- Review
- A novel, rapid and sensitive flow cytometry method reveals degradation of promoter proximal paused RNAPII in the presence and absence of UV.Nucleic acids research · 2022Article
- Cellular fractionation reveals transcriptome responses of human fibroblasts to UV-C irradiation.Cell death & disease · 2022Article
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- Dissecting regulatory pathways for transcription recovery following DNA damage reveals a non-canonical function of the histone chaperone HIRA.Nature communications · 2021Article
- The Winged Helix Domain of CSB Regulates RNAPII Occupancy at Promoter Proximal Pause Sites.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Cockayne syndrome type B ATPase (CSB) belongs to the SwItch/Sucrose nonfermentable family. Its mutations are linked to Cockayne syndrome phenotypes and classically are thought to be caused by defects in transcription-coupled repair, a subtype of DNA repair. Here we show that after UV-C irradiation, immediate early genes such as activating transcription factor 3 (ATF3) are overexpressed. Although the ATF3 target genes, including dihydrofolate reductase (DHFR), were unable to recover RNA synthesis in CSB-deficient cells, transcription was restored rapidly in normal cells. There the synthesis of DHFR mRNA restarts on the arrival of RNA polymerase II and CSB and the subsequent release of ATF3 from its cAMP response element/ATF target site. In CSB-deficient cells ATF3 remains bound to the promoter, thereby preventing the arrival of polymerase II and the restart of transcription. Silencing of ATF3, as well as stable introduction of wild-type CSB, restores RNA synthesis in UV-irradiated CSB cells, suggesting that, in addition to its role in DNA repair, CSB activity likely is involved in the reversal of inhibitory properties on a gene-promoter region. We present strong experimental data supporting our view that the transcriptional defects observed in UV-irradiated CSB cells are largely the result of a permanent transcriptional repression of a certain set of genes in addition to some defect in DNA repair.
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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.