Activation of PKCdelta by tyrosine phosphorylation in rat parotid acinar cells.
10.3346/jkms.2000.15.S.S40
- Author:
Cyril BENES
1
;
Yue ZHENG
;
Stephen P SOLTOFF
Author Information
1. Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston 02115, USA.
- Publication Type:Research Support, U.S. Gov't, P.H.S.
- Keywords:
PKC;
Parotid;
Tyrosine Phosphorylation;
Carbachol
- MeSH:
Animal;
Enzyme Activation/physiology;
Isoenzymes/metabolism*;
Male;
Parotid Gland/enzymology*;
Phosphorylation;
Protein Kinase C/metabolism*;
Rats;
Rats, Sprague-Dawley;
Tyrosine/metabolism*
- From:Journal of Korean Medical Science
2000;15(Suppl):S40-S41
- CountryRepublic of Korea
- Language:English
-
Abstract:
Receptor- and nonreceptor-mediated stimuli produce increases in both PKCdelta tyrosine phosphorylation and activity in rat parotid acinar cells and other cells. In vivo and in vitro increases and decreases in tyrosine phosphorylation resulted in increases and decreases, respectively, of PKCdelta activity. These studies demonstrated that increases in PKCdelta activity by G protein-coupled receptors and other stimuli were controlled by alterations in tyrosine phosphorylation.
