ArticleCell cycle (Georgetown, Tex.)2011
Involvement of the nuclear proteasome activator PA28γ in the cellular response to DNA double-strand breaks.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- Proteasomal-dependent CHK1 degradation leads to DNA damage accumulation in ALS cellular model systems.Cell death & disease · 2026Article
- PSME3 regulates migration and differentiation of myoblasts.Life science alliance · 2025Article
- Not Just PA28γ: What We Know About the Role of PA28αβ in Carcinogenesis.Biomolecules · 2025Review
- Proteasome-mediated degradation of long-range nucleases negatively regulates resection of DNA double-strand breaks.iScience · 2024Article
- PA200-Mediated Proteasomal Protein Degradation and Regulation of Cellular Senescence.International journal of molecular sciences · 2024Review
- Dynamic role of CUL4B in radiation-induced intestinal injury-regeneration.Scientific reports · 2024Article
- Structure, Function, and Allosteric Regulation of the 20S Proteasome by the 11S/PA28 Family of Proteasome Activators.Biomolecules · 2023Review
- Regulation of Life & Death by REGγ.Cells · 2022Review
- Histone degradation by the proteasome regulates chromatin and cellular plasticity.The FEBS journal · 2022Review
- PA28γ-20S proteasome is a proteolytic complex committed to degrade unfolded proteins.Cellular and molecular life sciences : CMLS · 2021Article
- LEDGF/p75 Is Required for an Efficient DNA Damage Response.International journal of molecular sciences · 2021Article
- PA28γ: New Insights on an Ancient Proteasome Activator.Biomolecules · 2021Review
- Radiation Exposure of Peripheral Mononuclear Blood Cells Alters the Composition and Function of Secreted Extracellular Vesicles.International journal of molecular sciences · 2020Article
- Article
- [Construction of an oral squamous cell carcinoma cell line for stable PA28γ overexpression].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2020Article
- PA28γ, an Accomplice to Malignant Cancer.Frontiers in oncology · 2020Review
- Silencing PSME3 induces colorectal cancer radiosensitivity by downregulating the expression of cyclin B1 and CKD1.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- Cellular Responses to Proteasome Inhibition: Molecular Mechanisms and Beyond.International journal of molecular sciences · 2019Review
- Regulation of Proteasome Activity by (Post-)transcriptional Mechanisms.Frontiers in molecular biosciences · 2019Review
- Visualizing Proteasome Activity and Intracellular Localization Using Fluorescent Proteins and Activity-Based Probes.Frontiers in molecular biosciences · 2019Article
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12 authors at 5 institutions in 3 countries.
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Abstract
The DNA damage response (DDR) is a complex signaling network that leads to damage repair while modulating numerous cellular processes. DNA double-strand breaks (DSBs), a highly cytotoxic DNA lesion, activate this system most vigorously. The DSB response network is orchestrated by the ATM protein kinase, which phosphorylates key players in its various branches. Proteasome-mediated protein degradation plays an important role in the proteome dynamics following DNA damage induction. Here, we identify the nuclear proteasome activator PA28γ (REGγ; PSME3) as a novel DDR player. PA28γ depletion leads to cellular radiomimetic sensitivity and a marked delay in DSB repair. Specifically, PA28γ deficiency abrogates the balance between the two major DSB repair pathways--nonhomologous end-joining and homologous recombination repair. Furthermore, PA28γ is found to be an ATM target, being recruited to the DNA damage sites and required for rapid accumulation of proteasomes at these sites. Our data reveal a novel ATM-PA28γ-proteasome axis of the DDR that is required for timely coordination of DSB repair.
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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.