N. Hirasawa et al., NEGATIVE REGULATION OF MAP-KINASE BY DIACYLGLYCEROL-DEPENDENT MECHANISMS VIA G-PROTEIN-COUPLED RECEPTORS IN RAT BASOPHILIC RBL-2H3(M1)-CELLS, Cellular signalling, 9(3-4), 1997, pp. 319-322
Carbachol and 5'-(N-ethylcarboxamido)-adenosine (NECA), stimulants of
G protein-coupled receptors, induce MAP kinase activation in the musca
rinic ml receptor-transfected mast cell line, RBL-2H3 (mi) cells. The
phospholipase C inhibitor neomycin and the phosphatidate phosphohydrol
ase inhibitor propranolol augmented MAP kinase activation induced by c
arbachol and NECA without affecting the antigen-induced MAP kinase act
ivation. Furthermore, the duration of MAP kinase activation induced by
carbachol or NECA was also prolonged by neomycin and propranolol. The
specific protein kinase C inhibitor Po 31-8425 enhanced the carbachol
- or NECA-induced MAP kinase activation. These findings suggest that t
he MAP kinase activation mediated by the G protein coupled receptors i
s negatively regulated by diacylglycerol and activated protein kinase
C(s). (C) 1997 Elsevier Science Inc.