ArticleNucleic acids research2016
Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo.
Article in Nucleic acids research, 2016. 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, 23 citations in OpenAlex.
- Article
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisNAR cancer · 2026Article
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisbioRxiv : the preprint server for biology · 2025Article
- Activation of FANCC attenuates mitochondrial ROS-driven necroptosis by targeting TBK1-dependent mitophagy in astrocytes after spinal cord injury.Theranostics · 2025Article
- The Role of Ubiquitination in Osteosarcoma Development and Therapies.Biomolecules · 2024Review
- RAD18 O-GlcNAcylation promotes translesion DNA synthesis and homologous recombination repair.Cell death & disease · 2024Article
- Role of Rad18 in B cell activation and lymphomagenesis.Scientific reports · 2024Article
- Impacts of arsenic on Rad18 and translesion synthesis.Toxicology and applied pharmacology · 2022Article
- Genome-wide CRISPR screen identified Rad18 as a determinant of doxorubicin sensitivity in osteosarcoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Growing and aging of hematopoietic stem cells.World journal of stem cells · 2021Review
- Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsNAR cancer · 2021Article
- DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Review
- RAD6 promotes chemoresistance in ovarian cancer.Molecular & cellular oncology · 2018Article
- DNA repair factor RAD18 and DNA polymerase Polκ confer tolerance of oncogenic DNA replication stress.The Journal of cell biology · 2017Article
- DNA damage tolerance in hematopoietic stem and progenitor cells in mice.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mechanisms of Post-Replication DNA Repair.Genes · 2017Review
- Accumulation of DNA damage in the aged hematopoietic stem cell compartment.Seminars in hematology · 2017Review
- Nrf2 Deficiency Brings About Increased Sensitive to IR and 7,12-dimethylbenz(a)anthracene and Leukemia Predisposition.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
In cultured cancer cells the E3 ubiquitin ligase Rad18 activates Trans-Lesion Synthesis (TLS) and the Fanconi Anemia (FA) pathway. However, physiological roles of Rad18 in DNA damage tolerance and carcinogenesis are unknown and were investigated here. Primary hematopoietic stem and progenitor cells (HSPC) co-expressed RAD18 and FANCD2 proteins, potentially consistent with a role for Rad18 in FA pathway function during hematopoiesis. However, hematopoietic defects typically associated with fanc-deficiency (decreased HSPC numbers, reduced engraftment potential of HSPC, and Mitomycin C (MMC) -sensitive hematopoiesis), were absent in Rad18(-/-) mice. Moreover, primary Rad18(-/-) mouse embryonic fibroblasts (MEF) retained robust Fancd2 mono-ubiquitination following MMC treatment. Therefore, Rad18 is dispensable for FA pathway activation in untransformed cells and the Rad18 and FA pathways are separable in hematopoietic cells. In contrast with responses to crosslinking agents, Rad18(-/-) HSPC were sensitive to in vivo treatment with the myelosuppressive agent 7,12 Dimethylbenz[a]anthracene (DMBA). Rad18-deficient fibroblasts aberrantly accumulated DNA damage markers after DMBA treatment. Moreover, in vivo DMBA treatment led to increased incidence of B cell malignancy in Rad18(-/-) mice. These results identify novel hematopoietic functions for Rad18 and provide the first demonstration that Rad18 confers DNA damage tolerance and tumor-suppression in a physiological setting.
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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.