ArticleCell regeneration (London, England)2025
Prmt5 is essential for intestinal stem cell maintenance and homeostasis.
Article in Cell regeneration (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Integrated inference of cellular compositions and gene expression programs by deconvolution.Cell regeneration (London, England) · 2026Article
- Protein Arginine Methyltransferase 6 Regulated Odontogenic Differentiation and Mitochondrial Function of Stem Cells from Apical Papilla Through its Nuclear Localization Sequence via β-catenin Pathway.International dental journal · 2026Article
- Emerging role of protein arginine methyltransferase 5 in gastrointestinal cancer (Review).Oncology letters · 2026Review
- Arginine Di-methylation of RIP3 safeguards necroptosis for intestinal homeostasis.Cell death and differentiation · 2026Article
- Lgr5⁺ cells regulate small intestinal morphogenesis before villification.Cell regeneration (London, England) · 2026Article
- PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.Stem cell research & therapy · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Intestinal homeostasis relies on the continuous renewal of intestinal stem cells (ISCs), which could be epigenetically regulated. While protein arginine methyltransferase 5 (Prmt5) is known to play a key role in multiple organs as an epigenetic modifier, its specific function in maintaining intestinal homeostasis remains to be elucidated. Here, we show that Prmt5 is highly expressed in mouse crypts. The deletion of Prmt5 results in ISCs deficiency, ectopic localization of Paneth cells, and spontaneous colitis. Mechanistically, Prmt5 sustains a high level of H3K27ac accumulation by inhibiting Hdac9 expression in the intestinal epithelium, and maintains the stemness of ISCs in a cell-autonomous manner. Notably, inhibition of histone deacetylases can rescue both self-renewal and differentiation capacities of Prmt5-depleted ISCs. These findings highlight Prmt5 as a critical regulator in intestinal epithelium development and tissue homeostasis.
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Registered trials
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