摘要
平滑肌收缩的原发信号一般来自肌浆中游离Ｃａ２＋浓度的增高．在调钙蛋白（Ｃａｌｍｏｄｕｌｉｎ，ＣａＭ）参与下，肌球蛋白轻链激酶（ＭＬＣＫ）被激活，从而催化肌球蛋白的磷酸化，启动平滑肌的横桥循环（ｃｒｏｓｓｂｒｉｄｇｅｃｙｃｌｉｎｇ）．除平滑肌收缩的钙依赖性调控外，也存在非钙依赖性调控的生化机理．这一条信号转导途径，可经由Ｇ蛋白以激活非钙依赖性蛋白激酶Ｃ的同工酶ＰＫＣ－ε，其下游步骤有两种钙结合蛋白（ｃａｌｐｏｎｉｎＣａＰ与Ｃａｌｄｅｓｍｏｎ，ＣａＤ）发挥了直接或间接靶蛋白的重要作用．
An elevation of sarcoplasmic free Ca 2+ concentration ([Ca 2+ ] i ) usually constitutes the primary signal for smooth muscle contraction.With the participation of calmodu lin,myosin light chain kinase (MLCK) is activated.Thus it catalyses myosin phosphorylation and triggers the crossbridge cycling in smooth muscle.In addition to Ca 2+ dependent regulation of smooth muscle contraction,also exists the biochemical mechanism of Ca 2+ independent regulation.This signal transduction pathway involves the activation of Ca 2+ independent isoenzyme of PKC(PKC ε) via G proteins.Two Ca 2+ binding proteins calponin(CaP) and caldesmon (CaD) have played important roles of direct or indirect target proteins in its downstream steps.
出处
《生命科学研究》
CAS
CSCD
1998年第3期157-162,共6页
Life Science Research
关键词
平滑肌
收缩
非钙依赖性
钙结合蛋白
smooth muscle,contraction(Ca 2+ independent),calponin,caldesmon
