Classical, novel and atypical isoforms of PKC stimulate ANF- and TRE/AP-1-regulated-promoter activity in ventricular cardiomyocytes.
FEBS Lett
; 356(2-3): 275-8, 1994 Dec 19.
Article
em En
| MEDLINE
| ID: mdl-7805853
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-alpha, novel PKC-epsilon or atypical PKC-zeta) 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-alpha, nPKC-epsilon or aPKC-zeta 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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
/
Expressão Gênica
/
Regiões Promotoras Genéticas
/
Proteínas Proto-Oncogênicas c-jun
/
Fator Natriurético Atrial
/
Isoenzimas
/
Miocárdio
Limite:
Animals
Idioma:
En
Ano de publicação:
1994
Tipo de documento:
Article