ArticleNucleic acids research2024
The dimeric deubiquitinase USP28 integrates 53BP1 and MYC functions to limit DNA damage.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- USP4 promotes non-small cell lung cancer tumorigenesis by antagonizing CNOT4-mediated degradation of PAF1.Respiratory research · 2026Article
- Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026Review
- Targeting the deubiquitinase USP28 in cancer: navigating context-dependent mechanisms and therapeutic resistance.Frontiers in immunology · 2026Review
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Molecular Mechanisms of the Ubiquitin-Specific Proteases (USPs) Family in Biliary Tract Cancer and Targeted Intervention Strategies.Biomedicines · 2025Review
- Deubiquitinase USP28 promotes the malignant progression and radio-resistance of hepatocellular carcinoma by stabilizing WDHD1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- USP28 promotes PARP inhibitor resistance by enhancing SOX9-mediated DNA damage repair in ovarian cancer.Cell death & disease · 2025Article
- Regulation of p53 by the mitotic surveillance/stopwatch pathway: implications in neurodevelopment and cancer.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
DNA replication is a major source of endogenous DNA damage in tumor cells and a key target of cellular response to genotoxic stress. DNA replication can be deregulated by oncoproteins, such as transcription factor MYC, aberrantly activated in many human cancers. MYC is stringently regulated by the ubiquitin system - for example, ubiquitination controls recruitment of the elongation factor PAF1c, instrumental in MYC activity. Curiously, a key MYC-targeting deubiquitinase USP28 also controls cellular response to DNA damage via the mediator protein 53BP1. USP28 forms stable dimers, but the biological role of USP28 dimerization is unknown. We show here that dimerization limits USP28 activity and restricts recruitment of PAF1c by MYC. Expression of monomeric USP28 stabilizes MYC and promotes PAF1c recruitment, leading to ectopic DNA synthesis and replication-associated DNA damage. USP28 dimerization is stimulated by 53BP1, which selectively binds USP28 dimers. Genotoxic stress diminishes 53BP1-USP28 interaction, promotes disassembly of USP28 dimers and stimulates PAF1c recruitment by MYC. This triggers firing of DNA replication origins during early response to genotoxins and exacerbates DNA damage. We propose that dimerization of USP28 prevents ectopic DNA replication at transcriptionally active chromatin to maintain genome stability.
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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.