ArticleNucleic acids research2014
PRMT5-mediated histone H4 arginine-3 symmetrical dimethylation marks chromatin at G + C-rich regions of the mouse genome.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Systemic administration of the PRMT5 inhibitor GSK3326595 does not induce overt cardiotoxicity in the murine heart.Journal of molecular and cellular cardiology plus · 2026Article
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- The Role of PRMT5 in Embryonic Developmental Arrest: Insights from IVF-ET Discarded Human Embryos.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Role of PRMT1 and PRMT5 in Breast Cancer.International journal of molecular sciences · 2024Review
- Histone H3 serine-57 is a CHK1 substrate whose phosphorylation affects DNA repair.Nature communications · 2023Article
- A type II protein arginine methyltransferase regulates merozoite invasion in Plasmodium falciparum.Communications biology · 2023Article
- Exploiting PRMT5 as a target for combination therapy in mantle cell lymphoma characterized by frequent ATM and TP53 mutations.Blood cancer journal · 2023Article
- Differential enrichment of H3K9me3 in intrahepatic cholangiocarcinoma.BMC medical genomics · 2022Article
- Review
- Human-specific gene CT47 blocks PRMT5 degradation to lead to meiosis arrest.Cell death discovery · 2022Article
- The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression.Molecular cancer · 2022Article
- An enhancer variant at 16q22.1 predisposes to hepatocellular carcinoma via regulating PRMT7 expression.Nature communications · 2022Article
- Transposable element regulation and expression in cancer.The FEBS journal · 2022Review
- The Novel Protease Activities of JMJD5-JMJD6-JMJD7 and Arginine Methylation Activities of Arginine Methyltransferases Are Likely Coupled.Biomolecules · 2022Review
- A First-in-Class, Highly Selective and Cell-Active Allosteric Inhibitor of Protein Arginine Methyltransferase 6.Journal of medicinal chemistry · 2021Article
- Symmetrical dimethylation of H4R3: A bridge linking DNA damage and repair upon oxidative stress.Redox biology · 2020Article
- PRMT5 Prevents Cardiomyocyte Hypertrophy via Symmetric Dimethylating HoxA9 and Repressing HoxA9 Expression.Frontiers in pharmacology · 2020Article
- Islet-specific Prmt5 excision leads to reduced insulin expression and glucose intolerance in mice.The Journal of endocrinology · 2020Article
- PRMT5-dependent transcriptional repression of c-Myc target genes promotes gastric cancer progression.Theranostics · 2020Article
- Review
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Symmetrical dimethylation on arginine-3 of histone H4 (H4R3me2s) has been reported to occur at several repressed genes, but its specific regulation and genomic distribution remained unclear. Here, we show that the type-II protein arginine methyltransferase PRMT5 controls H4R3me2s in mouse embryonic fibroblasts (MEFs). In these differentiated cells, we find that the genome-wide pattern of H4R3me2s is highly similar to that in embryonic stem cells. In both the cell types, H4R3me2s peaks are detected predominantly at G + C-rich regions. Promoters are consistently marked by H4R3me2s, independently of transcriptional activity. Remarkably, H4R3me2s is mono-allelic at imprinting control regions (ICRs), at which it marks the same parental allele as H3K9me3, H4K20me3 and DNA methylation. These repressive chromatin modifications are regulated independently, however, since PRMT5-depletion in MEFs resulted in loss of H4R3me2s, without affecting H3K9me3, H4K20me3 or DNA methylation. Conversely, depletion of ESET (KMT1E) or SUV420H1/H2 (KMT5B/C) affected H3K9me3 and H4K20me3, respectively, without altering H4R3me2s at ICRs. Combined, our data indicate that PRMT5-mediated H4R3me2s uniquely marks the mammalian genome, mostly at G + C-rich regions, and independently from transcriptional activity or chromatin repression. Furthermore, comparative bioinformatics analyses suggest a putative role of PRMT5-mediated H4R3me2s in chromatin configuration in the nucleus.
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