ArticleNature communications2017
ATM and CDK2 control chromatin remodeler CSB to inhibit RIF1 in DSB repair pathway choice.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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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
44 citing papers in PubMed, 73 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- OV16 Improves Radiation-Induced Intestinal Injury by Targeting Transglutaminase 2.Molecules (Basel, Switzerland) · 2026Article
- Transcription-Coupled Repair Promotes the Retention of Mutations in Coding Regions During Replication Stress.International journal of molecular sciences · 2026Article
- Metabolic Responses to Cyclic Fasting in Juvenile Turbot (Aquaculture nutrition · 2026Article
- Review
- Molecular basis for CSB stimulation of the SNM1A DNA repair nuclease.Research square · 2025Article
- Whole Blood DNA Methylation Analysis Reveals Epigenetic Changes Associated with ARSACS.Cerebellum (London, England) · 2025Article
- Perspectives in the investigation of Cockayne syndrome group B neurological disease: the utility of patient-derived brain organoid models.Journal of Zhejiang University. Science. B · 2024Review
- 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
- CircCDYL2 bolsters radiotherapy resistance in nasopharyngeal carcinoma by promoting RAD51 translation initiation for enhanced homologous recombination repair.Journal of experimental & clinical cancer research : CR · 2024Article
- Preimplantation genetic testing for Cockayne syndrome with a novel ERCC6 variant in a Chinese family.Frontiers in genetics · 2024Article
- RNAPII response to transcription-blocking DNA lesions in mammalian cells.The FEBS journal · 2023Review
- Untousling the Role of Tousled-like Kinase 1 in DNA Damage Repair.International journal of molecular sciences · 2023Review
- 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
- Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect.Life science alliance · 2023Article
- Lipodystrophy-associated progeroid syndromes.Hormones (Athens, Greece) · 2022Review
- A novel heterozygous ERCC6 variant identified in a Chinese family with non-syndromic primary ovarian insufficiency.Molecular genetics & genomic medicine · 2022Article
- Role of Cockayne Syndrome Group B Protein in Replication Stress: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
CSB, a member of the SWI2/SNF2 superfamily, is implicated in DNA double-strand break (DSB) repair. However, how it regulates this repair process is poorly understood. Here we uncover that CSB interacts via its newly identified winged helix domain with RIF1, an effector of 53BP1, and that this interaction mediates CSB recruitment to DSBs in S phase. At DSBs, CSB remodels chromatin by evicting histones, which limits RIF1 and its effector MAD2L2 but promotes BRCA1 accumulation. The chromatin remodeling activity of CSB requires not only damage-induced phosphorylation on S10 by ATM but also cell cycle-dependent phosphorylation on S158 by cyclin A-CDK2. Both modifications modulate the interaction of the CSB N-terminal region with its ATPase domain, the activity of which has been previously reported to be autorepressed by the N-terminal region. These results suggest that ATM and CDK2 control the chromatin remodeling activity of CSB in the regulation of DSB repair pathway choice.
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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.