ArticleOncogene2015
K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- A ubiquitin chain-feeding mechanism for BRCA1-A.Nature communications · 2026Article
- Efficacy of toripalimab in combination with anlotinib in recurrent undifferentiated pleomorphic sarcoma of the sinonasal region: a case report with biomarker analysis.Frontiers in immunology · 2025Article
- A comprehensive study evaluating germline FANCG variants in predisposition to breast and ovarian cancer.Cancer medicine · 2024Article
- Role of K63-linked ubiquitination in cancer.Cell death discovery · 2022Review
- Article
- DNA damage response and cancer therapeutics through the lens of the Fanconi Anemia DNA repair pathway.Cell communication and signaling : CCS · 2017Review
- Article
- Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.Cellular and molecular life sciences : CMLS · 2016Review
- The Lys63-deubiquitylating Enzyme BRCC36 Limits DNA Break Processing and Repair.The Journal of biological chemistry · 2016Article
- Tankyrases Promote Homologous Recombination and Check Point Activation in Response to DSBs.PLoS genetics · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA interstrand crosslinks (ICLs) are extremely deleterious lesions that are repaired by homologous recombination (HR) through coordination of Fanconi anemia (FA) proteins and breast cancer susceptibility gene 1 (BRCA1) product, but the exact role these proteins have remains unclear. Here we report that FANCG was modified by the addition of lysine63-linked polyubiquitin chains (K63Ub) in response to DNA damage. We show that FANCG K63Ub was dispensable for monoubiquitination of FANCD2, but was required for FANCG to interact with the Rap80-BRCA1 (receptor-associated protein 80-BRCA1) complex for subsequent modulation of HR repair of ICLs induced by mitomycin C. Mutation of three lysine residues within FANCG to arginine (K182, K258 and K347, 3KR) reduced FANCG K63Ub modification, as well as its interaction with the Rap80-BRCA1 complex, and therefore impeded HR repair. In addition, we demonstrated that K63Ub-modified FANCG was deubiquitinated by BRCC36 complex in vitro and in vivo. Inhibition of BRCC36 resulted in increased K63Ub modification of FANCG. Taken together, our results identify a new role of FANCG in HR repair of ICL through K63Ub-mediated interaction with the Rap80-BRCA1 complex.
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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.