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首页> 外文期刊>Biophysics >Regulation of Ca~(2+) Influx in Proliferating and Differentiating Murine Myoblasts with Participation of L-type Ca~(2+) Channels
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Regulation of Ca~(2+) Influx in Proliferating and Differentiating Murine Myoblasts with Participation of L-type Ca~(2+) Channels

机译:参与L型Ca〜(2+)通道的Ca〜(2+)内流在增生和分化鼠成肌细胞中的调控

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摘要

The basic mechanisms of regulation of Ca~(2+) influx have been studied in murine myoblasts prolif erating and differentiating in culture. The presence of Ltype Ca~(2+) channels in proliferating myoblasts is shown for the first time. It is also shown that the influx of Ca~(2+) through these channels is regulated by the adrenergic system. The influx of Ca~(2+) after activation of the adrenergic system by addition of adrenaline has been estimated in comparison with the contribution of reticular stocks exhausted by ATP in calciumfree medium. The Ca~(2+) influx in proliferating myoblasts is regulated by β2 adrenergic receptors whose action is mediated by adenylate cyclase through Ltype calcium channels. In differentiating myoblasts, the adrena lineinduced Ca~(2+) influx is substantially lower than in proliferating cells, and maximal influx of Ca~(2+) may be reached only upon exhaustion of reticular stocks.
机译:研究了Ca〜(2+)内流调节的基本机制在培养过程中增殖和分化的小鼠成肌细胞中。首次显示在成肌细胞中存在L型Ca〜(2+)通道。还表明,Ca〜(2+)通过这些通道的流入受肾上腺素能系统调节。与无钙培养基中ATP消耗的网状储备的贡献相比,估计了添加肾上腺素激活肾上腺素系统后Ca〜(2+)的流入。 β2肾上腺素能受体调节增殖的成肌细胞中的Ca〜(2+)流入,其作用由通过L型钙通道的腺苷酸环化酶介导。在分化成肌细胞中,肾上腺素诱导的Ca〜(2+)流入明显低于增殖细胞,并且仅在网状储备耗尽时才能达到Ca〜(2+)的最大流入。

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