ArticleProceedings of the National Academy of Sciences of the United States of America2002
Translocation of Cockayne syndrome group A protein to the nuclear matrix: possible relevance to transcription-coupled DNA repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 127 citations in OpenAlex.
- Analysis of cytosine deamination events in excision repair sequencing reads reveals mechanisms of incision site selection in NER.Nucleic acids research · 2024Article
- RNAPII response to transcription-blocking DNA lesions in mammalian cells.The FEBS journal · 2023Review
- DNA damage-induced transcription stress triggers the genome-wide degradation of promoter-bound Pol II.Nature communications · 2022Article
- Transcription-coupled nucleotide excision repair is coordinated by ubiquitin and SUMO in response to ultraviolet irradiation.Nucleic acids research · 2020Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- FACT subunit Spt16 controls UVSSA recruitment to lesion-stalled RNA Pol II and stimulates TC-NER.Nucleic acids research · 2019Article
- Regulation of the Intranuclear Distribution of the Cockayne Syndrome Proteins.Scientific reports · 2018Article
- Multiomic Analysis of the UV-Induced DNA Damage Response.Cell reports · 2016Article
- Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome.Journal of molecular biology · 2016Article
- The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair.The Journal of biological chemistry · 2016Article
- Melanocortin 1 Receptor: Structure, Function, and Regulation.Frontiers in genetics · 2016Review
- DNA repair mechanisms in dividing and non-dividing cells.DNA repair · 2013Review
- Oxidative DNA damage and nucleotide excision repair.Antioxidants & redox signaling · 2013Review
- KIAA1530 protein is recruited by Cockayne syndrome complementation group protein A (CSA) to participate in transcription-coupled repair (TCR).The Journal of biological chemistry · 2012Article
- Mutations in UVSSA cause UV-sensitive syndrome and destabilize ERCC6 in transcription-coupled DNA repair.Nature genetics · 2012Article
- BRCA1 contributes to transcription-coupled repair of DNA damage through polyubiquitination and degradation of Cockayne syndrome B protein.Cancer science · 2011Article
- The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome.Cell cycle (Georgetown, Tex.) · 2011Article
- Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging.The Journal of experimental medicine · 2010Article
- A UV-sensitive syndrome patient with a specific CSA mutation reveals separable roles for CSA in response to UV and oxidative DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Transcription-coupled repair (TCR) efficiently removes a variety of lesions from the transcribed strand of active genes. By allowing rapid resumption of RNA synthesis, the process is of major importance for cellular resistance to transcription-blocking genotoxic damage. Mutations in the Cockayne syndrome group A or B (CSA or CSB) gene result in defective TCR. However, the exact mechanism of TCR in mammalian cells remains to be elucidated. We found that CSA protein is rapidly translocated to the nuclear matrix after UV irradiation. The translocation of CSA was independent of Xeroderma pigmentosum group C, which is specific to the global genome repair subpathway of nucleotide excision repair (NER) and of the core NER factor Xeroderma pigmentosum group A but required the CSB protein. In UV-irradiated cells, CSA protein colocalized with the hyperphosphorylated form of RNA polymerase II, engaged in transcription elongation. The translocation of CSA was also induced by treatment of the cells with cisplatin or hydrogen peroxide, both of which produce damage that is subjected to TCR but not induced by treatment with dimethyl sulfate, which produces damage that is not subjected to TCR. The hydrogen peroxide-induced translocation of CSA was also CSB dependent. These findings establish a link between TCR and the nuclear matrix mediated by CSA.
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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.