ArticleMolecular and cellular biology2011
Pirh2 E3 ubiquitin ligase monoubiquitinates DNA polymerase eta to suppress translesion DNA synthesis.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Human DNA polymerase η is regulated by mutually exclusive mono-ubiquitination and mono-NEDDylation.Nucleic acids research · 2026Article
- Review
- SARS-CoV-2 and the DNA damage response.The Journal of general virology · 2023Review
- Polymerase η Recruits DHX9 Helicase to Promote Replication across Guanine Quadruplex Structures.Journal of the American Chemical Society · 2022Article
- The Role of E3 Ligase Pirh2 in Disease.Cells · 2022Review
- DNA Damage Tolerance Pathways in Human Cells: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
- Review
- Multisite SUMOylation restrains DNA polymerase η interactions with DNA damage sites.The Journal of biological chemistry · 2020Article
- Phosphorylation Alters the Properties of Pol η: Implications for Translesion Synthesis.iScience · 2018Article
- Polη O-GlcNAcylation governs genome integrity during translesion DNA synthesis.Nature communications · 2017Article
- The Translesion Polymerase Pol η Is Required for Efficient Epstein-Barr Virus Infectivity and Is Regulated by the Viral Deubiquitinating Enzyme BPLF1.Journal of virology · 2017Article
- Phosphorylation regulates human polη stability and damage bypass throughout the cell cycle.Nucleic acids research · 2017Article
- Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017Review
- Review
- Review
- Regulation of Mammalian DNA Replication via the Ubiquitin-Proteasome System.Advances in experimental medicine and biology · 2017Review
- MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo.Journal of molecular endocrinology · 2016Article
- The Regulation of DNA Damage Tolerance by Ubiquitin and Ubiquitin-Like Modifiers.Frontiers in genetics · 2016Review
- Functions of Ubiquitin and SUMO in DNA Replication and Replication Stress.Frontiers in genetics · 2016Review
- Protein monoubiquitylation: targets and diverse functions.Genes to cells : devoted to molecular & cellular mechanisms · 2015Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Polymerase eta (PolH) is necessary for translesion DNA synthesis, and PolH deficiency predisposes xeroderma pigmentosum variant (XPV) patients to cancer. Due to the critical role of PolH in translesion DNA synthesis, the activity of PolH is tightly controlled and subjected to multiple regulations, especially posttranslational modifications. Here, we show that PolH-dependent lesion bypass and intracellular translocation are regulated by Pirh2 E3 ubiquitin ligase through monoubiquitination. Specifically, we show that Pirh2, a target of the p53 tumor suppressor, monoubiquitinates PolH at one of multiple lysine residues. We also show that monoubiquitination of PolH inhibits the ability of PolH to interact with PCNA and to bypass UV-induced lesions, leading to decreased viability of UV-damaged cells. Moreover, we show that monoubiquitination of PolH alters the ability of PolH to translocate to replication foci for translesion DNA synthesis of UV-induced DNA lesions. Considering that Pirh2 is known to be overexpressed in various cancers, we postulate that in addition to mutation of PolH in XPV patients, inactivation of PolH by Pirh2 via monoubiquitination is one of the mechanisms by which PolH function is controlled, which might be responsible for the development and progression of some spontaneous tumors wherein PolH is not found to be mutated.
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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.