ArticleThe Journal of investigative dermatology2016
MEP50/PRMT5 Reduces Gene Expression by Histone Arginine Methylation and this Is Reversed by PKCδ/p38δ Signaling.
Article in The Journal of investigative dermatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Cryo-EM structure-based discovery of etravirine as a specific inhibitor of PRMT5/pICln protein-protein interaction for prostate cancer treatment.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Epidermal Loss of PRMT5 Leads to the Emergence of an Atypical Basal Keratinocyte-Like Cell Population and Defective Epidermal Stratification.The Journal of investigative dermatology · 2025Article
- Discovery and Biological Characterization of PRMT5:MEP50 Protein-Protein Interaction Inhibitors.Journal of medicinal chemistry · 2022Article
- PRMT5: a putative oncogene and therapeutic target in prostate cancer.Cancer gene therapy · 2022Review
- Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation.Computational and structural biotechnology journal · 2022Article
- Sulforaphane inhibits PRMT5 and MEP50 function to suppress the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2021Article
- Prmt5 promotes vascular morphogenesis independently of its methyltransferase activity.PLoS genetics · 2021Article
- The uncharacterized protein FAM47E interacts with PRMT5 and regulates its functions.Life science alliance · 2021Article
- Review
- Protein Arginine Methyltransferase 5 Promotes pICln-Dependent Androgen Receptor Transcription in Castration-Resistant Prostate Cancer.Cancer research · 2020Article
- PRMT5 Cooperates with pICln to Function as a Master Epigenetic Activator of DNA Double-Strand Break Repair Genes.iScience · 2020Article
- PRMT5 Prevents Cardiomyocyte Hypertrophy via Symmetric Dimethylating HoxA9 and Repressing HoxA9 Expression.Frontiers in pharmacology · 2020Article
- Cellular consequences of arginine methylation.Cellular and molecular life sciences : CMLS · 2019Review
- The methylation induced by protein arginine methyltransferase 5 promotes tumorigenesis and progression of lung cancer.Journal of thoracic disease · 2018Review
- Histone phosphorylation by TRPM6's cleaved kinase attenuates adjacent arginine methylation to regulate gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Myosin phosphatase and RhoA-activated kinase modulate arginine methylation by the regulation of protein arginine methyltransferase 5 in hepatocellular carcinoma cells.Scientific reports · 2017Article
- PRMT5 is essential for the maintenance of chondrogenic progenitor cells in the limb bud.Development (Cambridge, England) · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Protein kinase C δ (PKCδ) and p38δ are key proteins in a cascade that stimulates keratinocyte differentiation. This cascade activates transcription of involucrin (hINV) and other genes associated with differentiation. Protein arginine methyltransferase 5 (PRMT5) is an arginine methyltransferase that symmetrically dimethylates arginine residues. This protein interacts with a cofactor, methylosome protein 50 (MEP50), and symmetrically dimethylates arginine eight of histone 3 (H3R8me2s) and arginine three of histone 4 (H4R3me2s) to silence gene expression. We use the hINV gene as a tool to understand the relationship between PKCδ/p38δ and PRMT5/MEP50 signaling. MEP50 suppresses hINV mRNA level and promoter activity. This is associated with increased arginine dimethylation of hINV gene-associated H3/H4. We further show that the PKCδ/p38δ keratinocyte differentiation cascade reduces PRMT5 and MEP50 expression, association with the hINV gene promoter, and H3R8me2s and H4R2me2s formation. We propose that PRMT5/MEP50-dependent methylation is an epigenetic mechanism that assists in silencing of hINV expression, and that PKCδ signaling activates gene expression by directly activating transcription and by suppressing PRMT5/MEP50-dependent arginine dimethylation of promoter-associated histones. This is an example of crosstalk between PKCδ/p38δ signaling and PRMT5/MEP50 epigenetic silencing.
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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.