Chronic neurohormonal stimulation can have direct adverse effects on the structure and function of the heart. Heart failure develops and progresses as a result of the deleterious changes. It is well established that phosphorylation of class II HDAC5 (histone deacetylase 5) is an important event in the transcriptional regulation of cardiac gene reprogramming that results in the hypertrophic growth response. To date, experimentation on phosphorylation-mediated translocation of HDAC5 has focused on the regulatory properties of PKD (protein kinase D) within intact cells. With regard to the potential role of PKD in myocardium, recent observations raise the possibility that PKD-mediated myocardial regulatory mechanisms may represent promising therapeutic avenues for the treatment of heart failure. The present review summarizes the most recent and important insights into the role of PKD in hypertrophic signalling pathways.
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February 2012
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Conference Article|
January 19 2012
Protein kinase D in the hypertrophy pathway
Yuan Yan Sin;
Yuan Yan Sin
1
1Molecular Pharmacology Group, Institute of Cardiovascular and Medical Science, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, U.K.
1To whom correspondence should be addressed (email y.sin.1@research.gla.ac.uk).
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George S. Baillie
George S. Baillie
1Molecular Pharmacology Group, Institute of Cardiovascular and Medical Science, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, U.K.
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Publisher: Portland Press Ltd
Received:
July 14 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2012 Biochemical Society
2012
Biochem Soc Trans (2012) 40 (1): 287–289.
Article history
Received:
July 14 2011
Citation
Yuan Yan Sin, George S. Baillie; Protein kinase D in the hypertrophy pathway. Biochem Soc Trans 1 February 2012; 40 (1): 287–289. doi: https://doi.org/10.1042/BST20110626
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