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Helmstadter KG, Ljubojevic-Holzer S, Wood BM, et al. CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes. Basic Res Cardiol. 2021;116(1):11doi: 10.1007/s00395-021-00850-2.
Helmstadter, K. G., Ljubojevic-Holzer, S., Wood, B. M., Taheri, K. D., Sedej, S., Erickson, J. R., Bossuyt, J., & Bers, D. M. (2021). CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes. Basic research in cardiology, 116(1), 11. https://doi.org/10.1007/s00395-021-00850-2
Helmstadter, Kathryn G, et al. "CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes." Basic research in cardiology vol. 116,1 (2021): 11. doi: https://doi.org/10.1007/s00395-021-00850-2
Helmstadter KG, Ljubojevic-Holzer S, Wood BM, Taheri KD, Sedej S, Erickson JR, Bossuyt J, Bers DM. CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes. Basic Res Cardiol. 2021 Feb 15;116(1):11. doi: 10.1007/s00395-021-00850-2. PMID: 33590335; PMCID: PMC7884572.
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Basic Res Cardiol. 2021 Feb 15;116(1):11. doi: 10.1007/s00395-021-00850-2.

CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes.

Basic research in cardiology

Kathryn G Helmstadter, Senka Ljubojevic-Holzer, Brent M Wood, Khanha D Taheri, Simon Sedej, Jeffrey R Erickson, Julie Bossuyt, Donald M Bers

Affiliations

  1. Department of Pharmacology, University of California, Genome Building Rm 3513, Davis, CA, 95616-8636, USA.
  2. Department of Pharmacology, University of California, Genome Building Rm 3513, Davis, CA, 95616-8636, USA. [email protected].
  3. Department of Cardiology, Medical University of Graz, Graz, Austria. [email protected].
  4. BioTechMed-Graz, Graz, Austria. [email protected].
  5. Department of Cardiology, Medical University of Graz, Graz, Austria.
  6. BioTechMed-Graz, Graz, Austria.
  7. Department of Physiology and HeartOtago, University of Otago, Dunedin, New Zealand.
  8. Department of Pharmacology, University of California, Genome Building Rm 3513, Davis, CA, 95616-8636, USA. [email protected].

PMID: 33590335 PMCID: PMC7884572 DOI: 10.1007/s00395-021-00850-2

Abstract

Nuclear histone deacetylase 4 (HDAC4) represses MEF2-mediated transcription, implicated in the development of heart failure. CaMKII-dependent phosphorylation drives nucleus-to-cytoplasm HDAC4 shuttling, but protein kinase A (PKA) is also linked to HDAC4 translocation. However, the interplay of CaMKII and PKA in regulating adult cardiomyocyte HDAC4 translocation is unclear. Here we sought to determine the interplay of PKA- and CaMKII-dependent HDAC4 phosphorylation and translocation in adult mouse, rabbit and human ventricular myocytes. Confocal imaging and protein analyses revealed that inhibition of CaMKII-but not PKA, PKC or PKD-raised nucleo-to-cytoplasmic HDAC4 fluorescence ratio (F

Keywords: Calcium-calmodulin-dependent protein kinase (CaMKII); Cardiac hypertrophy; Histone deacetylase 4 (HDAC4); Protein kinase A (PKA); Ventricular remodeling

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