ArticleMolecules and cells2017
HDAC11 Inhibits Myoblast Differentiation through Repression of MyoD-Dependent Transcription.
Article in Molecules and cells, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 46 citations in OpenAlex.
- Integrative analysis of CUT&Tag-seq and RNA-seq reveals widespread H3K27ac upregulation associated with the activation of muscle-growth-related transcriptional programs in broiler breast muscle.Poultry science · 2026Article
- MRG15 decline in aged/injured MuSCs hinders regeneration via differentiation defects.Cell regeneration (London, England) · 2026Article
- Single cell RNA sequencing analysis of mice hindlimb muscles identifies transcriptional heterogeneity in aging and physical frailty.Scientific reports · 2025Article
- The Functions and Regulatory Mechanisms of Histone Modifications in Skeletal Muscle Development and Disease.International journal of molecular sciences · 2025Review
- Transcriptional Expression of Histone Acetyltransferases and Deacetylases During the Recovery of Acute Exercise in Mouse Hippocampus.Journal of molecular neuroscience : MN · 2024Article
- Emerging role of HDAC11 in skeletal muscle biology.Frontiers in cell and developmental biology · 2024Article
- Article
- Post-translational regulation of muscle growth, muscle aging and sarcopenia.Journal of cachexia, sarcopenia and muscle · 2023Review
- Tcf7l2 in hepatocytes regulates de novo lipogenesis in diet-induced non-alcoholic fatty liver disease in mice.Diabetologia · 2023Article
- Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.International journal of molecular sciences · 2023Review
- Article
- Sarcopenia in liver cirrhosis: perspectives from epigenetics and microbiota.Frontiers in medicine · 2023Review
- The epigenetic regulatory effect of histone acetylation and deacetylation on skeletal muscle metabolism-a review.Frontiers in physiology · 2023Review
- Effects of Toxic AGEs (TAGE) on Human Health.Cells · 2022Review
- HDAC11, an emerging therapeutic target for metabolic disorders.Frontiers in endocrinology · 2022Review
- N-acetyl cysteine prevents arecoline-inhibited C2C12 myoblast differentiation through ERK1/2 phosphorylation.PloS one · 2022Article
- Non-coding RNAs in cancer-associated cachexia: clinical implications and future perspectives.Translational oncology · 2021Review
- Increased Histone Acetylation and Decreased Expression of Specific Histone Deacetylases in Ultraviolet-Irradiated and Intrinsically Aged Human Skin In Vivo.International journal of molecular sciences · 2021Article
- Cigarette smoke extract modulatesAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death.Diabetology & metabolic syndrome · 2020Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal differentiation of muscle is closely associated with aging (sarcopenia) and diseases such as cancer and type II diabetes. Thus, understanding the mechanisms that regulate muscle differentiation will be useful in the treatment and prevention of these conditions. Protein lysine acetylation and methylation are major post-translational modification mechanisms that regulate key cellular processes. In this study, to elucidate the relationship between myogenic differentiation and protein lysine acetylation/methylation, we performed a PCR array of enzymes related to protein lysine acetylation/methylation during C2C12 myoblast differentiation. Our results indicated that the expression pattern of HDAC11 was substantially increased during myoblast differentiation. Furthermore, ectopic expression of HDAC11 completely inhibited myoblast differentiation, concomitant with reduced expression of key myogenic transcription factors. However, the catalytically inactive mutant of HDAC11 (H142/143A) did not impede myoblast differentiation. In addition, wild-type HDAC11, but not the inactive HDAC11 mutant, suppressed MyoD-induced promoter activities of MEF2C and MYOG (Myogenin), and reduced histone acetylation near the E-boxes, the MyoD binding site, of the MEF2C and MYOG promoters. Collectively, our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.
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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.