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activity
The Rowett Research Institute, Bucksburn, Aberdeen, Scotland AB21 9SB
Rat soleus muscle
was denervated for 3 or 7 days, and total membrane protein kinase C
(PKC) activity and translocation and immunocytochemical localization of
PKC isoforms were examined. Dietary administration of clenbuterol
concomitant with denervation ameliorated the atrophic response and was
associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (
, 
, 
, 
, and µ)
detected in soleus muscle by Western immunoblotting, clenbuterol
treatment affected only the PKC- and PKC- forms. PKC- was
translocated to the membrane fraction upon denervation, and the
presence of clenbuterol increased membrane-bound PKC- and active
PKC- as assayed by Ser657 phosphorylation. PKC-
protein was downregulated upon denervation, and treatment with
clenbuterol further decreased both cytosolic and membrane levels.
Immunolocalization of PKC- showed differences for regulatory and
catalytic domains, with the latter showing fast-fiber type specificity.
The results suggest potential roles of PKC- and PKC- in the
mechanism of action of clenbuterol in alleviating denervation-induced atrophy.
skeletal muscle; 
-agonist; kinase activity
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