ArticleNucleic acids research2007
Human RAD18 is involved in S phase-specific single-strand break repair without PCNA monoubiquitination.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 65 citations in OpenAlex.
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
- RAS-RAF-miR-296-3p signaling axis increases Rad18 expression to augment radioresistance in pancreatic and thyroid cancers.Cancer letters · 2024Article
- Implication of E3 ligase RAD18 in UV-induced mutagenesis in human induced pluripotent stem cells and neuronal progenitor cells.Journal of radiation research · 2023Article
- Impacts of arsenic on Rad18 and translesion synthesis.Toxicology and applied pharmacology · 2022Article
- Class I HDAC overexpression promotes temozolomide resistance in glioma cells by regulating RAD18 expression.Cell death & disease · 2022Article
- Identification of Human Cell Cycle Phase Markers Based on Single-Cell RNA-Seq Data by Using Machine Learning Methods.BioMed research international · 2022Article
- SET1/MLL family of proteins: functions beyond histone methylation.Epigenetics · 2021Review
- Synthetic Lethality through the Lens of Medicinal Chemistry.Journal of medicinal chemistry · 2020Review
- High RAD18 Expression is Associated with Disease Progression and Poor Prognosis in Patients with Gastric Cancer.Annals of surgical oncology · 2020Article
- USP5 promotes epithelial-mesenchymal transition by stabilizing SLUG in hepatocellular carcinoma.Theranostics · 2019Article
- DNA repair protein Rad18 restricts LINE-1 mobility.Scientific reports · 2018Article
- miR-184 promotes cell proliferation in tongue squamous cell carcinoma by targeting SOX7.Oncology letters · 2018Article
- E3 ubiquitin ligase Bre1 couples sister chromatid cohesion establishment to DNA replication ineLife · 2017Article
- miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3.Oncology letters · 2017Article
- Rad18-dependent SUMOylation of human specialized DNA polymerase eta is required to prevent under-replicated DNA.Nature communications · 2016Article
- Article
- DNA damage responses in cancer stem cells: Implications for cancer therapeutic strategies.World journal of biological chemistry · 2015Article
- RAD18 activates the G2/M checkpoint through DNA damage signaling to maintain genome integrity after ionizing radiation exposure.PloS one · 2015Article
- DNA damage-specific deubiquitination regulates Rad18 functions to suppress mutagenesis.The Journal of cell biology · 2014Article
- Ubiquitin-specific protease 5 is required for the efficient repair of DNA double-strand breaks.PloS one · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Switching from a replicative to a translesion polymerase is an important step to further continue on replication at the site of DNA lesion. Recently, RAD18 (a ubiquitin ligase) was shown to monoubiquitinate proliferating cell nuclear antigen (PCNA) in cooperation with RAD6 (a ubiquitin-conjugating enzyme) at the replication-stalled sites, causing the polymerase switch. Analyzing RAD18-knockout (RAD18-/-) cells generated from human HCT116 cells, in addition to the polymerase switch, we found a new function of RAD18 for S phase-specific DNA single-strand break repair (SSBR). Unlike the case with polymerase switching, PCNA monoubiquitination was not necessary for the SSBR. When compared with wild-type HCT116 cells, RAD18-/- cells, defective in the repair of X-ray-induced chromosomal aberrations, were significantly hypersensitive to X-ray-irradiation and also to the topoisomerase I inhibitor camptothecin (CPT) capable of inducing single-strand breaks but were not so sensitive to the topoisomerase II inhibitor etoposide capable of inducing double-strand breaks. However, such hypersensitivity to CPT observed with RAD18-/- cells was limited to only the S phase due to the absence of the RAD18 S phase-specific function. Furthermore, the defective SSBR observed in S phase of RAD18-/- cells was also demonstrated by alkaline comet assay.
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