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动脉平滑肌收缩中的调节机制。

Regulatory mechanism in arterial smooth muscle contraction.

作者信息

Koizumi T, Ito Y, Ebashi S

出版信息

Recent Adv Stud Cardiac Struct Metab. 1976;11:185-91.

PMID:145628
Abstract

The regulatory mechanism in the aortic actomyosin system was studied. Superprecipitation of desensitized aortic myosin B was not exhibited even in the presence of Ca2+, but was observable only in the presence of native tropomyosin and Ca2+. Reconstituted actomyosin composed of pure aortic myosin and pure skeletal actin did not show superprecipitation. Addition of aortic native tropomyosin and Ca2+ caused a marked superprecipitation. The ATPase of reconstituted actomyosin was enhanced three- or fourfold by aortic native tropomyosin and Ca2+. The extent of superprecipitation of aortic myosin B did not show a biphasic type of response to Mg-ATP concentration. Thus, aortic native tropomyosin induces a real activation of the myosin, actin, and ATP system in the presence of Ca2+, in contrast with the case of skeletal native tropomyosin, which induces the depression of skeletal myosin-actin-ATP interaction in the absence of Ca2+.

摘要

对主动脉肌动球蛋白系统中的调节机制进行了研究。即使存在Ca2+,脱敏的主动脉肌球蛋白B也不会出现超沉淀现象,只有在存在天然原肌球蛋白和Ca2+时才会观察到超沉淀现象。由纯主动脉肌球蛋白和纯骨骼肌肌动蛋白组成的重组肌动球蛋白未显示超沉淀现象。添加主动脉天然原肌球蛋白和Ca2+会引起明显的超沉淀现象。主动脉天然原肌球蛋白和Ca2+可使重组肌动球蛋白的ATP酶活性提高三到四倍。主动脉肌球蛋白B的超沉淀程度对Mg-ATP浓度未表现出双相反应类型。因此,与骨骼肌天然原肌球蛋白在无Ca2+时会导致骨骼肌肌球蛋白-肌动蛋白-ATP相互作用受抑制的情况相反,主动脉天然原肌球蛋白在有Ca2+存在时会真正激活肌球蛋白、肌动蛋白和ATP系统。

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