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MINIREVIEW

-Cell Ca_V channel regulation in physiology and pathophysiology

The Rolf Luft Center for Diabetes Research, Karolinska Diabetes Center, Department of Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden

Submitted 29 January 2004 ; accepted in final form 17 September 2004

The -cell is equipped with at least six voltage-gated Ca²⁺ (Ca_V) channel ₁-subunits designated Ca_V1.2, Ca_V1.3, Ca_V2.1, Ca_V2.2, Ca_V2.3, and Ca_V3.1. These principal subunits, together with certain auxiliary subunits, assemble into different types of Ca_V channels conducting L-, P/Q-, N-, R-, and T-type Ca²⁺ currents, respectively. The -cell shares customary mechanisms of Ca_V channel regulation with other excitable cells, such as protein phosphorylation, Ca²⁺-dependent inactivation, and G protein modulation. However, the -cell displays some characteristic features to bring these mechanisms into play. In islet -cells, Ca_V channels can be highly phosphorylated under basal conditions and thus marginally respond to further phosphorylation. In -cell lines, Ca_V channels can be surrounded by tonically activated protein phosphatases dominating over protein kinases; thus their activity is dramatically enhanced by inhibition of protein phosphatases. During the last 10 years, we have revealed some novel mechanisms of -cell Ca_V channel regulation under physiological and pathophysiological conditions, including the involvement of exocytotic proteins, inositol hexakisphosphate, and type 1 diabetic serum. This minireview highlights characteristic features of customary mechanisms of Ca_V channel regulation in -cells and also reviews our studies on newly identified mechanisms of -cell Ca_V channel regulation.

exocytotic proteins; inositol hexakisphosphate; pancreatic -cell; type 1 diabetic serum; voltage-gated Ca²⁺ channels

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