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Modulation of map kinase signaling and growth characteristics by the overexpression of protein kinase C in NIH3T3 cells
Author(s) -
Chang YoonYoung,
Kim SooJung,
Park TaeKyu,
Kang ShinSung,
Ha Mahn Joon,
Mushinski J. Fredric,
Chun JangSoo
Publication year - 1998
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549800203362
Subject(s) - protein kinase c , platelet derived growth factor receptor , map kinase kinase kinase , mitogen activated protein kinase kinase , microbiology and biotechnology , mitogen activated protein kinase , map2k7 , gene isoform , ask1 , cyclin dependent kinase 9 , mapk7 , signal transduction , chemistry , biology , kinase , growth factor , protein kinase a , cyclin dependent kinase 2 , biochemistry , receptor , gene
This study was performed to examine effects of the overexpression of protein kinase C (PKC) isoforms (i.e., βI, βII, γ, δ,η, and ζ) mitogen‐activated protein (MAP) kinase (Erk‐1 and ‐2) signaling and growth characteristics of NIH3T3 cells. Phorbol ester (PMA) activated endogenous and ectopically expressed PKCα, βI, βII, γ, δ, ε, and η. 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.