Classical, novel and atypical isoforms of PKC stimulate ANF- and TRE/AP-1-regulated-promoter activity in ventricular cardiomyocytes

Decock, J. B.J., Gillespie-Brown, J., Parker, P. J., Sugden, P. H. and Fuller, S. J. (1994) Classical, novel and atypical isoforms of PKC stimulate ANF- and TRE/AP-1-regulated-promoter activity in ventricular cardiomyocytes. FEBS Letters, 356(2-3), pp. 275-278. (doi:10.1016/0014-5793(94)01283-0) (PMID:7805853)

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Abstract

Cultured neonatal rat ventricular myocytes were co-transfected with expression plasmids encoding protein kinase C (PKC) isoforms from each of the PKC subfamilies (classical PKC-α, novel PKC-ε or atypical PKC-ξ) together with an atrial natriuretic factor (ANF) reporter plasmid. Each PKC had been rendered constitutively active by a single Ala→Glu mutation or a small deletion in the inhibitory pseudosubstrate site. cPKC-α, nPKC-ε or aPKC-ξ expression plasmids each stimulated ANF-promoter activity and expression of a reporter gene under the control of a 12-O-tetradecanoylphorbol 13-acetate-response element (TRE). Upregulation of the ANF promoter is characteristic of the hypertrophic response in the heart ventricle and a TRE is present in the ANF promoter. Thus all subfamilies of PKC may have the potential to contribute to hypertrophic response in cardiomyocytes.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Brown, Dr Judith
Authors: Decock, J. B.J., Gillespie-Brown, J., Parker, P. J., Sugden, P. H., and Fuller, S. J.
College/School:College of Medical Veterinary and Life Sciences > Institute of Health and Wellbeing > Public Health
Journal Name:FEBS Letters
Publisher:Elsevier
ISSN:0014-5793
Copyright Holders:Copyright © 1994 Federation of European Biochemical Societies
First Published:First published in Febs Letters 356(2-3):275-278
Publisher Policy:Reproduced in accordance with the copyright policy of the publisher

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