ArticleCommunications biology2020
PRMT5 promotes DNA repair through methylation of 53BP1 and is regulated by Src-mediated phosphorylation.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- PRMT5 is a prognostic-related biomarker associated with the tumor immune microenvironment in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Arginine methylation of human DNA topoisomerase I by PRMT5 facilitates DNA relaxation.Nucleic acids research · 2026Article
- Targeting PRMTs Creates Vulnerability of DNA Double-Stand Break Repair Pathways, and Potentiates Chemotherapy Efficacy in TNBC.Cancer science · 2026Article
- PRMT5 inhibition impairs Fanconi Anemia pathway-mediated homologous recombination and enhances the antitumor efficacy of Temozolomide in glioblastoma.Cell death & disease · 2026Article
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Reversible arginine methylation regulates mitochondrial IDH2 activity: coordinated control by CARM1 and KDM3A/4A.Cell death & disease · 2026Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- PARP inhibitor and PRMT5 inhibitor synergy is independent of BRCA1/2 and MTAP status in breast cancer cells.Scientific reports · 2025Article
- Reversible arginine methylation of PI3KC2α controls mitotic spindle dynamics.Cell communication and signaling : CCS · 2025Article
- Multifaceted roles of CARM1 beyond histone arginine methylation.Experimental & molecular medicine · 2025Review
- Therapeutic targeting of protein arginine methyltransferases reduces breast cancer progression by disrupting angiogenic pathways.Biochemistry and biophysics reports · 2025Review
- Methionine Dependency and Restriction in Cancer: Exploring the Pathogenic Function and Therapeutic Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The expression of PRMT5 is associated with postoperative chemotherapeutic outcome in colon cancer.BMC cancer · 2025Article
- CARM1/PRMT4 facilitates XPF-ERCC1 heterodimer assembly and maintains nucleotide excision repair activity.Nucleic acids research · 2025Article
- Alpha-synuclein regulates nucleolar DNA double-strand break repair in melanoma.Science advances · 2025Article
- High PRMT5 levels, maintained by KEAP1 inhibition, drive chemoresistance in high-grade serous ovarian cancer.The Journal of clinical investigation · 2025Article
- CARM1 regulates tubulin autoregulation through PI3KC2α R175 methylation.Cell communication and signaling : CCS · 2025Article
- PRMT5 inhibition sensitizes glioblastoma tumor models to temozolomide.Research square · 2025Article
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
PRMT5 participates in various cellular processes, including transcription regulation, signal transduction, mRNA splicing, and DNA repair; however, its mechanism of regulation is poorly understood. Here, we demonstrate that PRMT5 is phosphorylated at residue Y324 by Src kinase, a negative regulator of its activity. Either phosphorylation or substitution of the Y324 residue suppresses PRMT5 activity by preventing its binding with the methyl donor S-adenosyl-L-methionine. Additionally, we show that PRMT5 activity is associated with non-homologous end joining (NHEJ) repair by methylating and stabilizing p53-binding protein 1 (53BP1), which promotes cellular survival after DNA damage. Src-mediated phosphorylation of PRMT5 and the subsequent inhibition of its activity during the DNA damage process blocks NHEJ repair, leading to apoptotic cell death. Altogether, our findings suggest that PRMT5 regulates DNA repair through Src-mediated Y324 phosphorylation in response to DNA damage.
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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.