ArticleNucleic acids research2021
The H3K36me2 methyltransferase NSD1 modulates H3K27ac at active enhancers to safeguard gene expression.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Antagonistic roles of histone H3 lysine methyltransferases dictate tumor immune surveillance.Nature communications · 2026Article
- Single cell CRISPR screen identifies antagonism between Nsd1-H3K36me2 and Ezh2-H3K27me3 orchestrates pluripotency transition.Stem cell reports · 2026Article
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks.International journal of molecular sciences · 2026Review
- NSD1 governs H3K36me2-mediated DNA methylation and drives endo-mesodermal differentiation of human iPSCs.Clinical epigenetics · 2026Article
- Epigenetic Regulation of Production Traits in Ruminants: Implications for Breeding and Selection.Biology · 2026Review
- Many faces of mammalian NSD methyltransferases.Cellular & molecular biology letters · 2026Review
- M1 macrophage exosomes induce ferroptosis via MiR-582-5p-mediated ZBTB10 suppression in sepsis-induced acute kidney injury.Archives of medical science : AMS · 2026Article
- KDM3B Predicts Expression Signature, Prognosis Value, and Immune Characteristics of Cancers: A Pan-Cancer Analysis.BioMed research international · 2026Article
- Dysregulation of HOXA genes in acute myeloid leukemia and targeted therapy.NPJ precision oncology · 2025Review
- NSD Family-Mediated H3K36 Methylation in Human Cancer: Mechanisms and Therapeutic Opportunities.Biomedicines · 2025Review
- Synergistic regulation by H3K36 and H3K27 methylation defines the chromatin landscape to control virulence and secondary metabolism in a fungal pathogen.Genome research · 2025Article
- Reversion of aortic valve cells calcification by activation of Notch signalling via histone acetylation induction.Signal transduction and targeted therapy · 2025Article
- Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification.Journal of cell communication and signaling · 2025Article
- Overgrowth-intellectual disability disorders: progress in biology, patient advocacy and innovative therapies.Disease models & mechanisms · 2025Review
- The length of the G1 phase is an essential determinant of H3K27me3 landscapes across diverse cell types.PLoS biology · 2025Article
- Sperm-borne mRNAs: potential roles in zygote genome activation and epigenetic inheritance.Open biology · 2025Article
- Epigenetic reprogramming in pediatric gliomas: from molecular mechanisms to therapeutic implications.Trends in cancer · 2024Review
- The H3.3K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.Molecular cell · 2024Article
- MAT2B regulates the protein level of MAT2A to preserve RNA N6-methyladenosine.Cell death & disease · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetics, especially histone marks, functions beyond the DNA sequences to regulate gene expression. Depletion of NSD1, which catalyzes H3K36me2, leads to both up- and down-regulation of gene expression, indicating NSD1 is associated with both active and repressed gene expression. It's known that NSD1 regulates the deposition and expansion of H3K27me3, a repressive mark for gene expression, to keep active gene transcription. However, how NSD1 functions to repress gene expression is largely unknown. Here, we find that, when NSD1 is knocked out in mouse embryonic stem cells (mESCs), H3K27ac increases correlatively with the decrease of H3K36me2 at active enhancers, which is associated with mesoderm differentiation genes, leading to elevated gene expression. Mechanistically, NSD1 recruits HDAC1, the deacetylase of H3K27ac, to chromatin. Moreover, HDAC1 knockout (KO) recapitulates the increase of H3K27ac at active enhancers as the NSD1 depletion. Together, we propose that NSD1 deposits H3K36me2 and recruits HDAC1 at active enhancers to serve as a 'safeguard', preventing further activation of active enhancer-associated genes.
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