ArticleThe Journal of biological chemistry2011
Spatiotemporally distinct protein kinase D activation in adult cardiomyocytes in response to phenylephrine and endothelin.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- The role of A-kinase anchoring proteins in cardiovascular diseases and recent advances.Frontiers in cell and developmental biology · 2025Review
- Protein Kinase D1 Regulates Cardiac Hypertrophy, Potassium Channel Remodeling, and Arrhythmias in Heart Failure.Journal of the American Heart Association · 2022Article
- Article
- Decoding the Cardiac Actions of Protein Kinase D Isoforms.Molecular pharmacology · 2021Review
- Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure.Nature communications · 2019Article
- Nuclear translocation of calmodulin in pathological cardiac hypertrophy originates from ryanodine receptor bound calmodulin.Journal of molecular and cellular cardiology · 2018Article
- Inflammation leads through PGE/EPEMBO molecular medicine · 2018Article
- Subcellular compartmentalization of proximal GαThe Journal of biological chemistry · 2018Article
- Protein kinase D activation induces mitochondrial fragmentation and dysfunction in cardiomyocytes.The Journal of physiology · 2018Article
- Acute and Chronic Effects of Protein Kinase-D Signaling on Cardiac Energy Metabolism.Frontiers in cardiovascular medicine · 2018Review
- β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.Journal of the American Heart Association · 2017Article
- Emergency Spatiotemporal Shift: The Response of Protein Kinase D to Stress Signals in the Cardiovascular System.Frontiers in pharmacology · 2017Review
- Quantitative Monitoring Spatiotemporal Activation of Ras and PKD1 Using Confocal Fluorescent Microscopy.Methods in molecular biology (Clifton, N.J.) · 2016Article
- ATP-Binding Cassette Transporter Structure Changes Detected by Intramolecular Fluorescence Energy Transfer for High-Throughput Screening.Molecular pharmacology · 2015Article
- Chasing cardiac physiology and pathology down the CaMKII cascade.American journal of physiology. Heart and circulatory physiology · 2015Review
- Roles and post-translational regulation of cardiac class IIa histone deacetylase isoforms.The Journal of physiology · 2015Review
- Regulation of phosphatidylinositol-specific phospholipase C at the nuclear envelope in cardiac myocytes.Journal of cardiovascular pharmacology · 2015Review
- Nuclear compartmentalization of α1-adrenergic receptor signaling in adult cardiac myocytes.Journal of cardiovascular pharmacology · 2015Review
- Article
- Calcium-mediated histone modifications regulate alternative splicing in cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Protein kinase D (PKD) is a nodal point in cardiac hypertrophic signaling. It triggers nuclear export of class II histone deacetylase (HDAC) and regulates transcription. Although this pathway is thought to be critical in cardiac hypertrophy and heart failure, little is known about spatiotemporal aspects of PKD activation at the myocyte level. Here, we demonstrate that in adult cardiomyocytes two important neurohumoral stimuli that induce hypertrophy, endothelin-1 (ET1) and phenylephrine (PE), trigger comparable global PKD activation and HDAC5 nuclear export, but via divergent spatiotemporal PKD signals. PE-induced HDAC5 export is entirely PKD-dependent, involving fleeting sarcolemmal PKD translocation (for activation) and very rapid subsequent nuclear import. In contrast, ET1 recruits and activates PKD that remains predominantly sarcolemmal. This explains why PE-induced nuclear HDAC5 export in myocytes is totally PKD-dependent, whereas ET1-induced HDAC5 export depends more prominently on InsP(3) and CaMKII signaling. Thus α-adrenergic and ET-1 receptor signaling via PKD in adult myocytes feature dramatic differences in cellular localization and translocation in mediating hypertrophic signaling. This raises new opportunities for targeted therapeutic intervention into distinct limbs of this hypertrophic signaling pathway.
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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.