ArticleThe Journal of biological chemistry2015
Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Epac1 increases myosin regulatory light-chain phosphorylation, energetic cost of contraction, and susceptibility to heart failure.PloS one · 2025Article
- Article
- Insights into posttranslational regulation of skeletal muscle contractile function by the acetyltransferases, p300 and CBP.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Review
- Cardiac Acetylation in Metabolic Diseases.Biomedicines · 2022Review
- Article
- Alterations of Lysine Acetylation Profile in Murine Skeletal Muscles Upon Exercise.Frontiers in aging neuroscience · 2022Article
- Protein acetylation in cardiac aging.Journal of molecular and cellular cardiology · 2021Review
- Acetylation of Sarcoplasmic and Myofibrillar Proteins were Associated with Ovine Meat Quality Attributes at Early Postmortem.Food science of animal resources · 2021Article
- Mechanosignaling pathways alter muscle structure and function by post-translational modification of existing sarcomeric proteins to optimize energy usage.Journal of muscle research and cell motility · 2021Article
- Lysine acetylation of F-actin decreases tropomyosin-based inhibition of actomyosin activity.The Journal of biological chemistry · 2020Article
- p300 and cAMP response element-binding protein-binding protein in skeletal muscle homeostasis, contractile function, and survival.Journal of cachexia, sarcopenia and muscle · 2020Article
- Obesity-mediated regulation of cardiac protein acetylation: parallel analysis of total and acetylated proteins via TMT-tagged mass spectrometry.Bioscience reports · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Histone deacetylase activity governs diastolic dysfunction through a nongenomic mechanism.Science translational medicine · 2018Article
- Valproic acid disrupts the biomechanics of late spinal neural tube closure in mouse embryos.Mechanisms of development · 2018Article
- HDAC1 localizes to the mitochondria of cardiac myocytes and contributes to early cardiac reperfusion injury.Journal of molecular and cellular cardiology · 2018Article
- Inhibition of HDAC3 prevents diabetic cardiomyopathy in OVE26 mice via epigenetic regulation of DUSP5-ERK1/2 pathway.Clinical science (London, England : 1979) · 2017Article
- Dissociation of muscle insulin sensitivity from exercise endurance in mice by HDAC3 depletion.Nature medicine · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Reversible lysine acetylation is a widespread post-translational modification controlling the activity of proteins in different subcellular compartments. We previously demonstrated that a class II histone deacetylase (HDAC), HDAC4, and a histone acetyltransferase, p300/CREB-binding protein-associated factor, associate with cardiac sarcomeres and that a class I and II HDAC inhibitor, trichostatin A, enhances contractile activity of myofilaments. In this study we show that a class I HDAC, HDAC3, is also present at cardiac sarcomeres. By immunohistochemical and electron microscopic analyses, we found that HDAC3 was localized to A-band of sarcomeres and capable of deacetylating myosin heavy chain (MHC) isoforms. The motor domains of both cardiac α- and β-MHC isoforms were found to be reversibly acetylated. Biomechanical studies revealed that lysine acetylation significantly decreased the Km for the actin-activated ATPase activity of MHC isoforms. By in vitro motility assay, we found that lysine acetylation increased the actin-sliding velocity of α-myosin by 20% and β-myosin by 36% compared with their respective non-acetylated isoforms. Moreover, myosin acetylation was found to be sensitive to cardiac stress. During induction of hypertrophy, myosin isoform acetylation increased progressively with duration of stress stimuli independently of isoform shift, suggesting that lysine acetylation of myosin could be an early response of myofilaments to increase contractile performance of the heart. These studies provide the first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating the motor activity of cardiac MHC isoforms.
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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.