ArticleInternational journal of molecular sciences2016
Histone H3 Methyltransferase Suv39h1 Prevents Myogenic Terminal Differentiation by Repressing MEF2 Activity in Muscle Cells.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Biodegradation of short-chain phthalate esters (PAEs) by Sinomonas sp. S2 isolated from a soil contaminated by metal(loid)s smelting.Biodegradation · 2025Article
- The SUV39 Family of H3K9 Methyltransferases in Skeletal Muscle Stem Cells.FASEB bioAdvances · 2025Review
- Integrative ATAC-seq and RNA-seq Analysis of the Longissimus Dorsi Muscle of Gannan Yak and Jeryak.International journal of molecular sciences · 2024Article
- Epigenetic Regulation of Myogenesis: Focus on the Histone Variants.International journal of molecular sciences · 2021Review
- Regulation of proline-directed kinases and the trans-histone code H3K9me3/H4K20me3 during human myogenesis.The Journal of biological chemistry · 2019Article
- Myogenic regulatory factors: The orchestrators of myogenesis after 30 years of discovery.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- MEF2 signaling and human diseases.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The myogenic regulatory factors (MRFs) and myocyte enhancer factor 2 (MEF2) transcription factors have been extensively studied as key transcription factors that regulate myogenic gene expression. However, few reports on the molecular mechanism that modulates chromatin remodeling during skeletal muscle differentiation are available. We reported here that the expression of the H3-K9 methyltransferase Suv39h1 was decreased during myoblast differentiation. Ectopic expression of Suv39h1 could inhibit myoblast differentiation, increasing H3-K9 methylation levels, whereas knockdown of Suv39h1 stimulated myoblast differentiation. Furthermore, Suv39h1 interacted with MEF2C directly and inhibited MEF2 transcription activity in a dose-dependent manner. Together, our studies revealed a molecular mechanism wherein Suv39h1 modulated myogenic gene expression and activation during skeletal muscle differentiation.
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Registered trials
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