ArticleNucleic acids research2015
CSB interacts with SNM1A and promotes DNA interstrand crosslink processing.
Article in Nucleic acids research, 2015. 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, 60 citations in OpenAlex.
- Transcription remodeling and stalling by cisplatin-induced interstrand crosslinks.Nature chemical biology · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Molecular basis for CSB stimulation of the SNM1A DNA repair nuclease.Research square · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- Article
- Interstrand crosslinking of homologous repair template DNA enhances gene editing in human cells.Nature biotechnology · 2023Article
- Deploying solid-phase synthesis to access thymine-containing nucleoside analogs that inhibit DNA repair nuclease SNM1A.Organic & biomolecular chemistry · 2023Article
- Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023Review
- Role of Cockayne Syndrome Group B Protein in Replication Stress: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- Genetics behind Cerebral Disease with Ocular Comorbidity: Finding Parallels between the Brain and Eye Molecular Pathology.International journal of molecular sciences · 2022Review
- Targeting the Interplay between HDACs and DNA Damage Repair for Myeloma Therapy.International journal of molecular sciences · 2021Review
- LEO1 is a partner for Cockayne syndrome protein B (CSB) in response to transcription-blocking DNA damage.Nucleic acids research · 2021Article
- Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Article
- Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.Progress in biophysics and molecular biology · 2020Review
- The SNM1A DNA repair nuclease.DNA repair · 2020Review
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Cockayne syndrome (CS) is a premature aging disorder characterized by photosensitivity, impaired development and multisystem progressive degeneration, and consists of two strict complementation groups, A and B. Using a yeast two-hybrid approach, we identified the 5'-3' exonuclease SNM1A as one of four strong interacting partners of CSB. This direct interaction was confirmed using purified recombinant proteins-with CSB able to modulate the exonuclease activity of SNM1A on oligonucleotide substrates in vitro-and the two proteins were shown to exist in a common complex in human cell extracts. CSB and SNM1A were also found, using fluorescently tagged proteins in combination with confocal microscopy and laser microirradiation, to be recruited to localized trioxsalen-induced ICL damage in human cells, with accumulation being suppressed by transcription inhibition. Moreover, SNM1A recruitment was significantly reduced in CSB-deficient cells, suggesting coordination between the two proteins in vivo. CSB-deficient neural cells exhibited increased sensitivity to DNA crosslinking agents, particularly, in a non-cycling, differentiated state, as well as delayed ICL processing as revealed by a modified Comet assay and γ-H2AX foci persistence. The results indicate that CSB coordinates the resolution of ICLs, possibly in a transcription-associated repair mechanism involving SNM1A, and that defects in the process could contribute to the post-mitotic degenerative pathologies associated with CS.
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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.