ArticleNucleic acids research2015
Ectopic expression of RNF168 and 53BP1 increases mutagenic but not physiological non-homologous end joining.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- PCNA-binding activity separates RNF168 functions in DNA replication and DNA double-stranded break signaling.Nucleic acids research · 2024Article
- E3 ligases: a ubiquitous link between DNA repair, DNA replication and human disease.The Biochemical journal · 2024Review
- UBE2D3 facilitates NHEJ by orchestrating ATM signalling through multi-level control of RNF168.Nature communications · 2024Article
- Comprehensive mapping of cell fates in microsatellite unstable cancer cells supports dual targeting of WRN and ATR.Genes & development · 2023Article
- Immediate-Early, Early, and Late Responses to DNA Double Stranded Breaks.Frontiers in genetics · 2022Review
- SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells.Nature communications · 2020Article
- Review
- Ectopic RNF168 expression promotes break-induced replication-like DNA synthesis at stalled replication forks.Nucleic acids research · 2020Article
- Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The nuclear structural protein NuMA is a negative regulator of 53BP1 in DNA double-strand break repair.Nucleic acids research · 2019Article
- BRCA1 Haploinsufficiency Is Masked by RNF168-Mediated Chromatin Ubiquitylation.Molecular cell · 2019Article
- Mechanism of 53BP1 activity regulation by RNA-binding TIRR and a designer protein.Nature structural & molecular biology · 2018Article
- Retroviral insertional mutagenesis implicates E3 ubiquitin ligase RNF168 in the control of cell proliferation and survival.Bioscience reports · 2017Article
- TIRR and 53BP1- partners in arms.Cell cycle (Georgetown, Tex.) · 2017Article
- Article
- Regulatory cross-talk determines the cellular levels of 53BP1 protein, a critical factor in DNA repair.The Journal of biological chemistry · 2017Article
- Article
- 53BP1 fosters fidelity of homology-directed DNA repair.Nature structural & molecular biology · 2016Article
- Role of Deubiquitinating Enzymes in DNA Repair.Molecular and cellular biology · 2016Review
- Repair Pathway Choices and Consequences at the Double-Strand Break.Trends in cell biology · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
DNA double strand breaks (DSBs) formed during S phase are preferentially repaired by homologous recombination (HR), whereas G1 DSBs, such as those occurring during immunoglobulin class switch recombination (CSR), are repaired by non-homologous end joining (NHEJ). The DNA damage response proteins 53BP1 and BRCA1 regulate the balance between NHEJ and HR. 53BP1 promotes CSR in part by mediating synapsis of distal DNA ends, and in addition, inhibits 5' end resection. BRCA1 antagonizes 53BP1 dependent DNA end-blocking activity during S phase, which would otherwise promote mutagenic NHEJ and genome instability. Recently, it was shown that supra-physiological levels of the E3 ubiquitin ligase RNF168 results in the hyper-accumulation of 53BP1/BRCA1 which accelerates DSB repair. Here, we ask whether increased expression of RNF168 or 53BP1 impacts physiological versus mutagenic NHEJ. We find that the anti-resection activities of 53BP1 are rate-limiting for mutagenic NHEJ but not for physiological CSR. As heterogeneity in the expression of RNF168 and 53BP1 is found in human tumors, our results suggest that deregulation of the RNF168/53BP1 pathway could alter the chemosensitivity of BRCA1 deficient tumors.
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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.