ArticleJournal of cell science2013
RNF168 forms a functional complex with RAD6 during the DNA damage response.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Crotonylation of MCM6 enhances chemotherapeutics sensitivity of breast cancer via inducing DNA replication stress.Cell proliferation · 2025Article
- PCNA-binding activity separates RNF168 functions in DNA replication and DNA double-stranded break signaling.Nucleic acids research · 2024Article
- The role of ubiquitin-conjugating enzyme in the process of spermatogenesis.Reproductive biology and endocrinology : RB&E · 2024Review
- Histone post-translational modification and the DNA damage response.Genes & diseases · 2023Review
- Next-Generation Sequencing in the Assessment of the Transcriptomic Landscape of DNA Damage Repair Genes in Abdominal Aortic Aneurysm, Chronic Venous Disease and Lower Extremity Artery Disease.International journal of molecular sciences · 2022Article
- BET-Inhibitor I-BET762 and PARP-Inhibitor Talazoparib Synergy in Small Cell Lung Cancer Cells.International journal of molecular sciences · 2020Article
- RAD6B is a major mediator of triple negative breast cancer cisplatin resistance: Regulation of translesion synthesis/Fanconi anemia crosstalk and BRCA1 independence.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- RAD6B Plays a Critical Role in Neuronal DNA Damage Response to Resist Neurodegeneration.Frontiers in cellular neuroscience · 2019Article
- L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage.Nature cell biology · 2018Article
- The mTOR-S6K pathway links growth signalling to DNA damage response by targeting RNF168.Nature cell biology · 2018Article
- Autophagy Roles in the Modulation of DNA Repair Pathways.International journal of molecular sciences · 2017Review
- An E2-guided E3 Screen Identifies the RNF17-UBE2U Pair as Regulator of the Radiosensitivity, Immunodeficiency, Dysmorphic Features, and Learning Difficulties (RIDDLE) Syndrome Protein RNF168.The Journal of biological chemistry · 2017Article
- USP51 deubiquitylates H2AK13,15ub and regulates DNA damage response.Genes & development · 2016Article
- Synthesis and in vitro anticancer evaluation of some 4,6-diamino-1,3,5-triazine-2-carbohydrazides as Rad6 ubiquitin conjugating enzyme inhibitors.Bioorganic & medicinal chemistry letters · 2016Article
- Systematic E2 screening reveals a UBE2D-RNF138-CtIP axis promoting DNA repair.Nature cell biology · 2015Article
- RNF8 deficiency results in neurodegeneration in mice.Neurobiology of aging · 2015Article
- RAD6 promotes homologous recombination repair by activating the autophagy-mediated degradation of heterochromatin protein HP1.Molecular and cellular biology · 2015Article
- UbcH7 regulates 53BP1 stability and DSB repair.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- 53BP1, BRCA1, and the choice between recombination and end joining at DNA double-strand breaks.Molecular and cellular biology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Protein ubiquitination plays an important role in initiating the DNA damage response. Following DNA damage, E2 ubiquitin conjugating enzymes are crucial for catalyzing substrate ubiquitination that recruits downstream DNA repair factors to DNA lesions. To identify novel E2 conjugating enzymes important for initiating the DNA-damage-induced ubiquitination cascade, we screened most of the known E2 enzymes and found that RAD6A and RAD6B function together with RNF168 in the ionizing radiation (IR)-induced DNA damage response. Similarly to RNF168-deficient cells, RAD6A- or RAD6B-deficient cells exhibit a reduction in DNA-damage-induced protein ubiquitination. Correspondingly, DNA-damage-induced foci formation of DNA damage repair proteins, such as BRCA1 and 53BP1, is impaired in the absence of RAD6A or RAD6B. Moreover, the RNF168-RAD6 complex targeted histone H1.2 for ubiquitination in vitro and regulated DNA-damage-induced histone H1.2 ubiquitination in vivo. Collectively, these data demonstrate that RNF168, in complex with RAD6A or RAD6B, is activated in the DNA-damage-induced protein ubiquitination cascade.
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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.