ArticleThe EMBO journal2015
Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 73 citations in OpenAlex.
- ASCC3 promotes chemosensitivity in colorectal cancer cells.Scientific reports · 2026Article
- Transcription-Coupled Repair Promotes the Retention of Mutations in Coding Regions During Replication Stress.International journal of molecular sciences · 2026Article
- Review
- A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence.Aging cell · 2025Article
- A Truncating Variant in theGenetics research · 2025Article
- Article
- CSB and SMARCAL1 compete for RPA32 at stalled forks and differentially control the fate of stalled forks in BRCA2-deficient cells.Nucleic acids research · 2024Article
- Article
- Transcriptional profiling of peripheral blood mononuclear cells identifies inflammatory phenotypes in Ataxia Telangiectasia.Orphanet journal of rare diseases · 2024Article
- CSB Regulates Pathway Choice in Response to DNA Replication Stress Induced by Camptothecin.International journal of molecular sciences · 2023Article
- DNA double-strand break genetic variants in patients with premature ovarian insufficiency.Journal of ovarian research · 2023Review
- Nuclear DJ-1 Regulates DNA Damage Repair via the Regulation of PARP1 Activity.International journal of molecular sciences · 2023Article
- Premature aging in genetic diseases: what conclusions can be drawn for physiological aging.Frontiers in aging · 2023Review
- 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
- Effects of Oxygen Tension for Membrane Lipidome Remodeling of Cockayne Syndrome Cell Models.Cells · 2022Article
- Cockayne syndrome group B protein regulates fork restart, fork progression and MRE11-dependent fork degradation in BRCA1/2-deficient cells.Nucleic acids research · 2021Article
- RNA Expression of DNA Damage Response Genes in Muscle-Invasive Bladder Cancer: Influence on Outcome and Response to Adjuvant Cisplatin-Based Chemotherapy.International journal of molecular sciences · 2021Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations of CSB account for the majority of Cockayne syndrome (CS), a devastating hereditary disorder characterized by physical impairment, neurological degeneration and segmental premature aging. Here we report the generation of a human CSB-knockout cell line. We find that CSB facilitates HR and represses NHEJ. Loss of CSB or a CS-associated CSB mutation abrogating its ATPase activity impairs the recruitment of BRCA1, RPA and Rad51 proteins to damaged chromatin but promotes the formation of 53BP1-Rif1 damage foci in S and G2 cells. Depletion of 53BP1 rescues the formation of BRCA1 damage foci in CSB-knockout cells. In addition, knockout of CSB impairs the ATM- and Chk2-mediated DNA damage responses, promoting a premature entry into mitosis. Furthermore, we show that CSB accumulates at sites of DNA double-strand breaks (DSBs) in a transcription-dependent manner. The kinetics of DSB-induced chromatin association of CSB is distinct from that of its UV-induced chromatin association. These results reveal novel, important functions of CSB in regulating the DNA DSB repair pathway choice as well as G2/M checkpoint activation.
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What OpenQuestion holds
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.