ArticleJournal of the American Heart Association2017
β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Epigenetic, neuroplasticity, and adrenergic targets associated with major depression in immune cells.Scientific reports · 2026Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- PP2A-B56α is a key determinant of cardiac protein phosphorylation and functional responses to β-adrenergic signalling.Journal of molecular and cellular cardiology plus · 2025Article
- Sex-specific regulation of the cardiac transcriptome by the protein phosphatase 2A regulatory subunit B55α.npj metabolic health and disease · 2024Article
- 14-3-3 binding motif phosphorylation disrupts Hdac4-organized condensates to stimulate cardiac reprogramming.Cell reports · 2024Article
- Article
- Physiological and pathological roles of protein kinase A in the heart.Cardiovascular research · 2022Review
- Quantitative Analysis of the Cardiac Phosphoproteome in Response to Acute β-Adrenergic Receptor Stimulation In Vivo.International journal of molecular sciences · 2021Article
- CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes.Basic research in cardiology · 2021Article
- Adaptive versus maladaptive cardiac remodelling in response to sustained β-adrenergic stimulation in a new 'ISO on/off model'.PloS one · 2021Article
- Regulation of histone deacetylase activities and functions by phosphorylation and its physiological relevance.Cellular and molecular life sciences : CMLS · 2021Review
- Protein phosphatase 2A-mediated flotillin-1 dephosphorylation up-regulates endothelial cell migration and angiogenesis regulation.The Journal of biological chemistry · 2019Article
- mAKAPβ signalosomes - A nodal regulator of gene transcription associated with pathological cardiac remodeling.Cellular signalling · 2019Review
- Role of type 2A phosphatase regulatory subunit B56α in regulating cardiac responses to β-adrenergic stimulation in vivo.Cardiovascular research · 2019Article
- Differential localizations of protein phosphatase 1 isoforms determine their physiological function in the heart.Acta biochimica et biophysica Sinica · 2019Article
- Inflammation leads through PGE/EPEMBO molecular medicine · 2018Article
- Bidirectional regulation of HDAC5 by mAKAPβ signalosomes in cardiac myocytes.Journal of molecular and cellular cardiology · 2018Article
- β-Adrenergic regulation of cardiac type 2A protein phosphatase through phosphorylation of regulatory subunit B56δ at S573.Journal of molecular and cellular cardiology · 2018Article
- New Aspects of Vascular Calcification: Histone Deacetylases and Beyond.Journal of Korean medical science · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundClass IIa histone deacetylase (HDAC) isoforms such as HDAC5 are critical signal-responsive repressors of maladaptive cardiomyocyte hypertrophy, through nuclear interactions with transcription factors including myocyte enhancer factor-2. β-Adrenoceptor (β-AR) stimulation, a signal of fundamental importance in regulating cardiac function, has been proposed to induce both phosphorylation-independent nuclear export and phosphorylation-dependent nuclear accumulation of cardiomyocyte HDAC5. The relative importance of phosphorylation at Ser259/Ser498 versus Ser279 in HDAC5 regulation is also controversial. We aimed to determine the impact of β-AR stimulation on the phosphorylation, localization, and function of cardiomyocyte HDAC5 and delineate underlying molecular mechanisms. METHODS AND
resultsA novel 3-dimensional confocal microscopy method that objectively quantifies the whole-cell nuclear/cytoplasmic distribution of green fluorescent protein tagged HDAC5 revealed the β-AR agonist isoproterenol to induce β
conclusionsβ-AR stimulation induces HDAC5 nuclear accumulation in cardiomyocytes by a mechanism that is protein kinase A-dependent but requires B55α-PP2A-mediated dephosphorylation of Ser259/Ser498 rather than protein kinase A-mediated phosphorylation of Ser279.
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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.