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KMID : 1206220040110010020
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Journal of Korean Academy of Physical Therapy Science
2004 Volume.11 No. 1 p.20 ~ p.27
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The Role of Actin Binding Protein -Caldesmon- of the Mechanism of -dependent/-independent Smooth Muscle Contraction - Approach of Basic Medical for the Study of Senile Cardiovascular Disease-related Senile Physical Therapy -
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Kim Jung-Hwan
Min Kyung-Ok
Choi Young-Deok
Lee Joon-Hee
Chon Ki-Young
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Abstract
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It is widely accepted that smooth muscle contraction is triggered by intracellular () released from intracellular stores such as sarcoplasmic reticulum (SR) and from the extracellular space, The increased can phosphorylate the 20-kDa myosin light chain () by activating MLC kinase (MLCK), and this initiates smooth muscle contraction. In addition to the -MLCK-tension pathway, a number of intracellular signal molecules, including mitogen-activated protein kinase (MAPK), protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), and Rho-associated coiled coil-forming protein kinase (ROCK), play important roles in the regulation of smooth muscle contraction. However, the mechanisms regulating contraction of caldesmon (CaD), actin-binding protein, are not entirely elucidated in the presence of . It is known that CaD tightly interacts with actin and inhibits actomyosin ATPase activity. Therefore, the purpose of the present study was to investigate the roles of -dependent CaD in smooth muscle contraction. Endothelin-1 (ET-1), G-protein coupled receptor agonist and vasoconstrictor, increased both vascular smooth contraction and phosphorylation of CaD in the presence of . These results suggest that ET-1 induces contraction and phosphorylation of CaD in rat aortic smooth muscle, which may he mediated by the increase of .
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KEYWORD
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Caldesmon (CaD), Muscle contraction, Intracellular, Mitogen-activated protein kinase (MAPK), Senile cardiovascular disease
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