ArticleCell death and differentiation2016
Splicing controls the ubiquitin response during DNA double-strand break repair.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.Nucleic acids research · 2022Pooled it
- RNA splicing in health and disease.Molecular biomedicine · 2026Review
- MUSICiAn: genome-wide identification of genes involved in DNA repair via control-free mutational spectra analysis.NAR genomics and bioinformatics · 2026Article
- Compound 7 h exerts its anti-oncogenic effects on colorectal cancer cells by inducing death-receptor-mediated apoptosis, promoting DNA damage, and obstructing autophagic flux.BMC pharmacology & toxicology · 2026Article
- KRT80, Regulated by RNF8-Mediated Ubiquitination, Contributes to Glucose Metabolic Reprogramming and Progression of Glioblastoma.Neurochemical research · 2025Article
- The translatome of glioblastoma.Molecular oncology · 2025Article
- Assessment of SF3B1 Expression as a Prognostic Marker for Neoadjuvant Chemotherapy Response in Stage III Triple-Negative Breast Cancer.Reports of biochemistry & molecular biology · 2025Article
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- Biochemistry and Protein Interactions of the CYREN Microprotein.Biochemistry · 2023Article
- Regulation of the hypertonic stress response by the 3' mRNA cleavage and polyadenylation complex.Genetics · 2023Article
- Article
- Development of Olaparib-Resistance Prostate Cancer Cell Lines to Identify Mechanisms Associated with Acquired Resistance.Cancers · 2022Article
- Therapeutic Targeting of Alternative Splicing: A New Frontier in Cancer Treatment.Frontiers in oncology · 2022Review
- Maturation State-Specific Alternative Splicing inCancers · 2021Article
- Nuclear WRAP53 promotes neuronal survival and functional recovery after stroke.Science advances · 2020Article
- The X-linked trichothiodystrophy-causing gene RNF113A links the spliceosome to cell survival upon DNA damage.Nature communications · 2020Article
- The roles of RNA in DNA double-strand break repair.British journal of cancer · 2020Review
- The Cajal Body Protein WRAP53β Prepares the Scene for Repair of DNA Double-Strand Breaks by Regulating Local Ubiquitination.Frontiers in molecular biosciences · 2019Review
- Transcriptomic rationale for synthetic lethality-targeting ERCC1 and CDKN1A in chronic myelomonocytic leukaemia.British journal of haematology · 2018Article
- From "Cellular" RNA to "Smart" RNA: Multiple Roles of RNA in Genome Stability and Beyond.Chemical reviews · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although evidence that splicing regulates DNA repair is accumulating, the underlying mechanism(s) remain unclear. Here, we report that short-term inhibition of pre-mRNA splicing by spliceosomal inhibitors impairs cellular repair of DNA double-strand breaks. Indeed, interference with splicing as little as 1 h prior to irradiation reduced ubiquitylation of damaged chromatin and impaired recruitment of the repair factors WRAP53β, RNF168, 53BP1, BRCA1 and RAD51 to sites of DNA damage. Consequently, splicing-deficient cells exhibited significant numbers of residual γH2AX foci, as would be expected if DNA repair is defective. Furthermore, we show that this is due to downregulation of the E3 ubiquitin ligase RNF8 and that re-introduction of this protein into splicing-deficient cells restores ubiquitylation at sites of DNA damage, accumulation of downstream factors and subsequent repair. Moreover, downregulation of RNF8 explains the defective repair associated with knockdown of various splicing factors in recent genome-wide siRNA screens and, significantly, overexpression of RNF8 counteracts this defect. These discoveries reveal a mechanism that may not only explain how splicing regulates repair of double-strand breaks, but also may underlie various diseases caused by deregulation of splicing factors, including cancer.
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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.