ArticleThe Journal of biological chemistry2010
Rad18-mediated translesion synthesis of bulky DNA adducts is coupled to activation of the Fanconi anemia DNA repair pathway.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- Deciphering the role of post-translational modifications in fanconi anemia proteins and their influence on tumorigenesis.Cancer gene therapy · 2024Review
- Case Report: SMARCA4 (BRG1)-deficient undifferentiated carcinoma of gallbladder with genetic analysis.Frontiers in oncology · 2023Article
- RAD18 opposes transcription-associated genome instability through FANCD2 recruitment.PLoS genetics · 2022Article
- Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022Review
- Impacts of arsenic on Rad18 and translesion synthesis.Toxicology and applied pharmacology · 2022Article
- FANCI plays an essential role in spermatogenesis and regulates meiotic histone methylation.Cell death & disease · 2021Article
- Cooperation of the ATM and Fanconi Anemia/BRCA Pathways in Double-Strand Break End Resection.Cell reports · 2020Article
- The DNA damage response acts as a safeguard against harmful DNA-RNA hybrids of different origins.EMBO reports · 2019Article
- Acetaldehyde forms covalent GG intrastrand crosslinks in DNA.Scientific reports · 2019Article
- A new look at molecular biology of breast cancer.Cancer biology & therapy · 2019Review
- FAM35A associates with REV7 and modulates DNA damage responses of normal and BRCA1-defective cells.The EMBO journal · 2018Article
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- FAN1 interaction with ubiquitylated PCNA alleviates replication stress and preserves genomic integrity independently of BRCA2.Nature communications · 2017Article
- FANCD2 and DNA Damage.International journal of molecular sciences · 2017Review
- Pharmacological targeting of RAD6 enzyme-mediated translesion synthesis overcomes resistance to platinum-based drugs.The Journal of biological chemistry · 2017Article
- A neomorphic cancer cell-specific role of MAGE-A4 in trans-lesion synthesis.Nature communications · 2016Article
- The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016Review
- Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo.Nucleic acids research · 2016Article
- FANCM interacts with PCNA to promote replication traverse of DNA interstrand crosslinks.Nucleic acids research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Fanconi anemia (FA) is a cancer susceptibility syndrome characterized by sensitivity to DNA-damaging agents. The FA proteins (FANCs) are implicated in DNA repair, although the precise mechanisms by which FANCs process DNA lesions are not fully understood. An epistatic relationship between the FA pathway and translesion synthesis (TLS, a post-replication DNA repair mechanism) has been suggested, but the basis for cross-talk between the FA and TLS pathways is poorly understood. We show here that ectopic overexpression of the E3 ubiquitin ligase Rad18 (a central regulator of TLS) induces DNA damage-independent mono-ubiquitination of proliferating cell nuclear antigen (PCNA) (a known Rad18 substrate) and FANCD2. Conversely, DNA damage-induced mono-ubiquitination of both PCNA and FANCD2 is attenuated in Rad18-deficient cells, demonstrating that Rad18 contributes to activation of the FA pathway. WT Rad18 but not an E3 ubiquitin ligase-deficient Rad18 C28F mutant fully complements both PCNA ubiquitination and FANCD2 activation in Rad18-depleted cells. Rad18-induced mono-ubiquitination of FANCD2 is not observed in FA core complex-deficient cells, demonstrating that Rad18 E3 ligase activity alone is insufficient for FANCD2 ubiquitylation. Instead, Rad18 promotes FA core complex-dependent FANCD2 ubiquitination in a manner that is secondary to PCNA mono-ubiquitination. Taken together, these results demonstrate a novel Rad18-dependent mechanism that couples activation of the FA pathway with TLS.
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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.