This study does not support the hypothesis that caldesmon function in vascular smooth muscle is modulated by phosphorylation.
Challenges hypothesis of phosphorylation modulating caldesmon in vascular smooth muscle; leaves open its physiological role pending in vivo confirmation.
Caldesmon was phosphorylated up to 1.2 molPi/mol using a partially purified endogenous kinase fraction. The phosphorylation site was within the C-terminal 99 amino acids. We were also able to phosphorylate caldesmon incorporated into native and synthetic smooth muscle thin filaments. Phosphorylation did not alter caldesmon binding to actin or inhibition of actomyosin ATPase. It also did not change Ca2+ sensitivity in native thin filaments. Phosphorylated caldesmon bound to myosin less than unphosphorylated caldesmon, especially when the myosin was also not phosphorylated. This work did not support the hypothesis that caldesmon function is modulated by phosphorylation.
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Pintér et al. (1992) studied this question.
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