RGK regulation of voltage-gated calcium channels
RGK regulation of voltage-gated calcium channels
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DOI：
10.1007/s11427-014-4788-x
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发表时间：
2015-01-01
影响因子：
9.1
通讯作者：
Yang Jian
中科院分区：
文献类型：
--
作者：
Buraei, Zafir;Lumen, Ellie;Yang Jian
电压门控钙通道 (VGCC) 在心脏和骨骼肌收缩、激素和神经递质释放以及细胞增殖、分化、迁移和死亡等较慢的过程中发挥着关键作用。 VGCC的突变会导致多种心脏、肌肉和神经系统疾病，其生理功能受到激酶、磷酸酶、G蛋白、钙调蛋白和许多其他蛋白质的严格调节。十五年前，RGK 蛋白被发现是 VGCC 最有效的内源性调节因子。它们是 Ras GTPases 超家族中的单体 GTPases 家族（Rad、Rem、Rem2 和 Gem/Kir），具有两个已知功能：调节细胞骨架动力学（包括树突状树枝化）和抑制 VGCC。在这里，我们回顾了 RGK 介导的 VGCC 抑制的机制和分子决定因素、这种抑制的生理影响，以及连接两种已知 RGK 功能的最新证据。
Voltage-gated calcium channels (VGCCs) play critical roles in cardiac and skeletal muscle contractions, hormone and neurotransmitter release, as well as slower processes such as cell proliferation, differentiation, migration and death. Mutations in VGCCs lead to numerous cardiac, muscle and neurological disease, and their physiological function is tightly regulated by kinases, phosphatases, G-proteins, calmodulin and many other proteins. Fifteen years ago, RGK proteins were discovered as the most potent endogenous regulators of VGCCs. They are a family of monomeric GTPases (Rad, Rem, Rem2, and Gem/Kir), in the superfamily of Ras GTPases, and they have two known functions: regulation of cytoskeletal dynamics including dendritic arborization and inhibition of VGCCs. Here we review the mechanisms and molecular determinants of RGK-mediated VGCC inhibition, the physiological impact of this inhibition, and recent evidence linking the two known RGK functions.