ArticlePloS one2014
Regulation of 53BP1 protein stability by RNF8 and RNF168 is important for efficient DNA double-strand break repair.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- An unexpected role of CLASP1 in radiation response and S-phase regulation of head and neck cancer cells.PloS one · 2025Article
- The Role of Protein Arginine Methyltransferases in DNA Damage Response.International journal of molecular sciences · 2022Review
- Mutations of the DNA repair gene PNKP in a patient with microcephaly, seizures, and developmental delay (MCSZ) presenting with a high-grade brain tumor.Scientific reports · 2022Article
- Defective repair of topoisomerase I induced chromosomal damage in Huntington's disease.Cellular and molecular life sciences : CMLS · 2022Article
- PRMT5 promotes DNA repair through methylation of 53BP1 and is regulated by Src-mediated phosphorylation.Communications biology · 2020Article
- PHF2 regulates homology-directed DNA repair by controlling the resection of DNA double strand breaks.Nucleic acids research · 2020Article
- CBP mediated DOT1L acetylation confers DOT1L stability and promotes cancer metastasis.Theranostics · 2020Article
- Review
- The nuclear interactome of DYRK1A reveals a functional role in DNA damage repair.Scientific reports · 2019Article
- Lipolytic inhibitor G0S2 modulates glioma stem-like cell radiation response.Journal of experimental & clinical cancer research : CR · 2019Article
- RNF8 mediates NONO degradation following UV-induced DNA damage to properly terminate ATR-CHK1 checkpoint signaling.Nucleic acids research · 2019Article
- Altered DNA repair; an early pathogenic pathway in Alzheimer's disease and obesity.Scientific reports · 2018Article
- Article
- PARP2 controls double-strand break repair pathway choice by limiting 53BP1 accumulation at DNA damage sites and promoting end-resection.Nucleic acids research · 2017Article
- Retroviral insertional mutagenesis implicates E3 ubiquitin ligase RNF168 in the control of cell proliferation and survival.Bioscience reports · 2017Article
- Differential requirements for DNA repair proteins in immortalized cell lines using alternative lengthening of telomere mechanisms.Genes, chromosomes & cancer · 2017Article
- CHD1 loss sensitizes prostate cancer to DNA damaging therapy by promoting error-prone double-strand break repair.Annals of oncology : official journal of the European Society for Medical Oncology · 2017Article
- Wwox-Brca1 interaction: role in DNA repair pathway choice.Oncogene · 2017Article
- RNF168 cooperates with RNF8 to mediate FOXM1 ubiquitination and degradation in breast cancer epirubicin treatment.Oncogenesis · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
53BP1 regulates DNA double-strand break (DSB) repair. In functional assays for specific DSB repair pathways, we found that 53BP1 was important in the conservative non-homologous end-joining (C-NHEJ) pathway, and this activity was dependent upon RNF8 and RNF168. We observed that 53BP1 protein was diffusely abundant in nuclei, and upon ionizing radiation, 53BP1 was everywhere degraded except at DNA damage sites. Depletion of RNF8 or RNF168 blocked the degradation of the diffusely localized nuclear 53BP1, and ionizing radiation induced foci (IRIF) did not form. Furthermore, when 53BP1 degradation was inhibited, a subset of 53BP1 was bound to DNA damage sites but bulk, unbound 53BP1 remained in the nucleoplasm, and localization of its downstream effector RIF1 at DSBs was abolished. Our data suggest a novel mechanism for responding to DSB that upon ionizing radiation, 53BP1 was divided into two populations, ensuring functional DSB repair: damage site-bound 53BP1 whose binding signal is known to be generated by RNF8 and RNF168; and unbound bulk 53BP1 whose ensuing degradation is regulated by RNF8 and RNF168.
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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.