Extracellular HIV-1 Tat protein induces a rapid and selective activation of protein kinase C (PKC)-alpha, and -epsilon and -zeta isoforms in PC12 cells.
Biochem Biophys Res Commun
; 242(2): 332-7, 1998 Jan 14.
Article
en En
| MEDLINE
| ID: mdl-9446795
ABSTRACT
The addition in culture of extracellular HIV-1 Tat protein (0.1-1 nM) to PC12 cells induced a rapid increase of the bulk protein kinase C (PKC) catalytic activity. Among various PKC isoforms (alpha, beta I, beta II, delta, epsilon, eta, theta, and zeta) expressed in PC12 cells, Tat selectively stimulated alpha, epsilon, and zeta, as judged by activities in immunoprecipitates. Activation of these isoforms was suppressed by the tyrosine kinase inhibitor genistein. Moreover, PKC-zeta showed the fastest kinetics of activation in response to Tat, but PKC-alpha and PKC-epsilon showed the highest levels of activation. PKC-alpha activation was accompanied by a rise of intracellular IP3, while the PI 3-kinase inhibitors wortmannin and LY294002 suppressed PKC-epsilon activation. Taken together, these findings demonstrate that extracellular Tat shows a cytokine-like activity in PC12 cells, being able to trigger an intracellular signalling cascade which involves PKC-alpha, -epsilon, and -zeta.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteína Quinasa C
/
Productos del Gen tat
/
VIH-1
Límite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
1998
Tipo del documento:
Article
País de afiliación:
Estados Unidos