ArticleNature communications2019
Genotoxic stress-triggered β-catenin/JDP2/PRMT5 complex facilitates reestablishing glutathione homeostasis.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 44 citations in OpenAlex.
- PRMT5 promotes ferroptosis in cisplatin-induced acute kidney injury through WDR5/ACSL4 pathway.Redox biology · 2026Article
- Emerging roles of protein arginine methyltransferase in multiple myeloma.Molecular therapy. Oncology · 2025Review
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Cuprorivaite microspheres inhibit cuproptosis and oxidative stress in osteoarthritis via Wnt/β-catenin pathway.Materials today. Bio · 2024Article
- ZMAT2 condensates regulate the alternative splicing of TRIM28 to reduce cellular ROS accumulation, thereby promoting the proliferation of HCC cells.Cell communication and signaling : CCS · 2024Article
- Mechanism of Histone Arginine Methylation Dynamic Change in Cellular Stress.International journal of molecular sciences · 2024Article
- YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD-L1/VEGFA Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis.Journal of neuroinflammation · 2024Review
- PRMT5 reduces immunotherapy efficacy in triple-negative breast cancer by methylating KEAP1 and inhibiting ferroptosis.Journal for immunotherapy of cancer · 2023Article
- Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review).International journal of oncology · 2023Review
- Modulation of Nrf2/HO-1 by Natural Compounds in Lung Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Targeting pre-mRNA splicing in cancers: roles, inhibitors, and therapeutic opportunities.Frontiers in oncology · 2023Review
- Protein arginine methylation in viral infection and antiviral immunity.International journal of biological sciences · 2023Review
- Inhibition of Wdr5 Attenuates Ang-II-Induced Fibroblast-to-Myofibroblast Transition in Cardiac Fibrosis by Regulating Mdm2/P53/P21 Pathway.Biomolecules · 2022Article
- Antioxidant Therapy in Cancer: Rationale and Progress.Antioxidants (Basel, Switzerland) · 2022Review
- HSF1 facilitates the multistep process of lymphatic metastasis in bladder cancer via a novel PRMT5-WDR5-dependent transcriptional program.Cancer communications (London, England) · 2022Article
- PRMT5: a putative oncogene and therapeutic target in prostate cancer.Cancer gene therapy · 2022Review
- Cellular pathways influenced by protein arginine methylation: Implications for cancer.Molecular cell · 2021Review
- Review
- Engineered Fibroblast Extracellular Vesicles Attenuate Pulmonary Inflammation and Fibrosis in Bleomycin-Induced Lung Injury.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying how cells subjected to genotoxic stress reestablish reduction-oxidation (redox) homeostasis to scavenge genotoxic stress-induced reactive oxygen species (ROS), which maintains the physiological function of cellular processes and cell survival, remain unclear. Herein, we report that, via a TCF-independent mechanism, genotoxic stress induces the enrichment of β-catenin in chromatin, where it forms a complex with ATM phosphorylated-JDP2 and PRMT5. This elicits histone H3R2me1/H3R2me2s-induced transcriptional activation by the recruitment of the WDR5/MLL methyltransferase complexes and concomitant H3K4 methylation at the promoters of multiple genes in GSH-metabolic cascade. Treatment with OICR-9429, a small-molecule antagonist of the WDR5-MLL interaction, inhibits the β-catenin/JDP2/PRMT5 complex-reestablished GSH metabolism, leading to a lethal increase in the already-elevated levels of ROS in the genotoxic-agent treated cancer cells. Therefore, our results unveil a plausible role for β-catenin in reestablishing redox homeostasis upon genotoxic stress and shed light on the mechanisms of inducible chemotherapy resistance in cancer.
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