Sustained muscle contraction induced by agonists, growth factors, and Ca2+mediated by distinct PKC isozymes

• DOI: 10.1152/ajpgi.2000.279.1.g201
• Publication Date: 2017-12-24T15:30:49Z
• Authors: K. S. Murthy; J. R. Grider; J. F. Kuemmerle; G. M. Makhlouf
• Keywords: Calphostin C; Chelerythrine; Calphostin; PKC alpha

The role of protein kinase C (PKC) in sustained contraction was examined intestinal circular and longitudinal muscle cells. Initial induced by agonists (CCK-8 neuromedin C) abolished 1) inhibitors Ca 2+ mobilization (neomycin dimethyleicosadienoic acid), 2) calmidazolium, 3) myosin light chain (MLC) (MLCK) inhibitor KT-5926. In contrast, not affected these but the PKC chelerythrine calphostin C, PKC-ε antibody, a pseudosubstrate inhibitor. GDPβS both initial contraction, whereas Gα q/11 antibody inhibited only implying that dependent on activation distinct G protein. Sustained epidermal growth factor PKC-α,β,γ PKC-α (0.4 μM) an permeabilized cells blocked calmodulin MLCK antibody. Thus , agonists, factors is mediated MLCK, specific -dependent -independent isozymes. protein-coupled receptors are linked to via proteins.