RGK regulation of voltage-gated calcium channels

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• 作者：Zafir Buraei (1)
  Ellie Lumen (1)
  Sukhjinder Kaur (1)
  Jian Yang (2) (3)
  
  1. Department of Biology ; Pace University ; New York ; NY ; 10038 ; USA
  2. Ion Channel Research and Drug Development Center ; and Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province ; Kunming Institute of Zoology ; Chinese Academy of Sciences ; Kunming ; 650223 ; China
  3. Department of Biological Sciences ; Columbia University ; New York ; NY ; 10027 ; USA
  
• 关键词：calcium ; channel modulation ; trafficking ; cardiac physiology ; neurobiology ; beta subunit
• 刊名：Science China Life Sciences
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：58
• 期：1
• 页码：28-38
• 全文大小：1,137 KB
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• 刊物主题：Life Sciences, general;
• 出版者：Springer Berlin Heidelberg
• ISSN：1869-1889

文摘

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.