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Modulation of MAP kinase signaling and growth characteristics by the overexpression of protein kinase C in NIH3T3 cells.

Authors
Chang, YY; Kim, SJ; Park, TK; Kang, SS; Ha, MJ; Mushinsk, JF; Chun, JS
Citation
Biochemistry and molecular biology international, 45(6):1139-1148, 1998
Journal Title
Biochemistry and molecular biology international
ISSN
1039-9712
Abstract
This study was performed to examine effects of the overexpression of protein kinase C (PKC) isoforms (i.e., beta I, beta II, gamma, delta, eta, and zeta) on mitogen-activated protein (MAP) kinase (Erk-1 and -2) signaling and growth characteristics of NIH3T3 cells. Phorbol ester (PMA) activated endogenous and ectopically expressed PKC alpha, beta I, beta II, gamma, delta, epsilon, and eta. Overexpression of the examined PKC isoforms enhanced PMA-induced MAP kinase activation. Potentiation of MAP kinase activation was also observed upon stimulation of cells with platelet-derived growth factor (PDGF) although there was no indication for the activation PKC isoforms by PDGF. Inhibition of PKC blocked PMA- but not PDGF-induced MAP kinase activation. Thus, potentiation of PDGF-induced MAP kinase activation appears to be independent to PKC activity, while PMA-induced MAP kinase activation requires PKC activity. The ability of PKC isoforms to potentiate MAP kinase activation is not related to the growth characteristics of cells because individual PKC isoforms differentially regulated maximum density and proliferation of cells.
MeSH terms
3T3 CellsAnimalsCalcium-Calmodulin-Dependent Protein Kinases/*physiologyCell Division/physiologyGene ExpressionMiceProtein Isoforms/physiologyProtein Kinase C/*biosynthesis/geneticsSignal Transduction/*physiology
PMID
9762412
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Anatomy
AJOU Authors
하, 만준
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