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Signaling regulatory mechanisms of the contractile activity of smooth muscle

机译:平滑肌收缩活动的信号调节机制

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A comparative model been designed to study a contribution of proteinkinase C-(PKC)-activated intracellular signaling pathways in generation of different contractile responses of vascular (tonic) and visceral (phasic) smooth muscles. We have determined that, in tonic smooth muscle, PKC mediates activation of MAP-kinases that phosphorylate key regulatory proteins of the contractile system, myosin light chain kinase and caldesmon, leading to upregulation of actomyosine motor activity. In contrast, the MAP-kinase activation is uncoupled from the contractile machinery in phasic smooth muscles, which also reveal high levels of myosin light chain kinase-related protein KRP that contributes to relaxation. Phosphorylation of KRP following activation of PKC or cyclic nucleotide-dependent protein kinases enhances the KRP activity and further contributes to relaxion in phasic smooth muscle. A possibility is discussed for exploitation of the comparative model described herein for investigation of specific role of other regulatory intracellular pathways in generation of vascular tonic contraction. myshts. zhurnal imeni I.M. Sechenova / Rossi inverted question markskaia akademiia nauk.
机译:设计了一个比较模型来研究蛋白激酶C-(PKC)激活的细胞内信号通路在血管(张力)和内脏(相位)平滑肌不同收缩反应的产生中的作用。我们已经确定,在强直性平滑肌中,PKC介导MAP激酶的激活,该磷酸化收缩系统的关键调节蛋白,肌球蛋白轻链激酶和Caldesmon,从而导致肌动蛋白运动活性的上调。相反,MAP激酶的激活与相位平滑肌的收缩机制无关,这也揭示了高水平的肌球蛋白轻链激酶相关蛋白KRP有助于放松。 PKC或环状核苷酸依赖性蛋白激酶激活后,KRP的磷酸化增强了KRP活性,并进一步促进了相位平滑肌的松弛。讨论了开发本文描述的比较模型的可能性,该比较模型用于研究其他调节性细胞内途径在血管补剂收缩产生中的特定作用。 myshts。 zhurnal imeni I.M. Sechenova / Rossi提出了反问号

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