ArticleCell cycle (Georgetown, Tex.)2016
Replication Protein A (RPA) deficiency activates the Fanconi anemia DNA repair pathway.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Phosphorylation by ATR triggers FANCD2 chromatin loading and activates the Fanconi anemia pathway.Cell reports · 2023Article
- The RPA inhibitor HAMNO sensitizes Fanconi anemia pathway-deficient cells.Cell cycle (Georgetown, Tex.) · 2022Article
- RPA3 is a potential marker of prognosis and radioresistance for nasopharyngeal carcinoma.Journal of cellular and molecular medicine · 2017Article
- Overlooked FANCD2 variant encodes a promising, portent tumor suppressor, and alternative polyadenylation contributes to its expression.Oncotarget · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
The Fanconi anemia (FA) pathway regulates DNA inter-strand crosslink (ICL) repair. Despite our greater understanding of the role of FA in ICL repair, its function in the preventing spontaneous genome instability is not well understood. Here, we show that depletion of replication protein A (RPA) activates the FA pathway. RPA1 deficiency increases chromatin recruitment of FA core complex, leading to FANCD2 monoubiquitination (FANCD2-Ub) and foci formation in the absence of DNA damaging agents. Importantly, ATR depletion, but not ATM, abolished RPA1 depletion-induced FANCD2-Ub, suggesting that ATR activation mediated FANCD2-Ub. Interestingly, we found that depletion of hSSB1/2-INTS3, a single-stranded DNA-binding protein complex, induces FANCD2-Ub, like RPA1 depletion. More interestingly, depletion of either RPA1 or INTS3 caused increased accumulation of DNA damage in FA pathway deficient cell lines. Taken together, these results indicate that RPA deficiency induces activation of the FA pathway in an ATR-dependent manner, which may play a role in the genome maintenance.
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