1887

Abstract

The Cch1 protein of the yeast is a homologue of the pore-forming subunit of mammalian voltage-gated Ca channels (VGCCs), and it constitutes a high-affinity Ca-influx system with the Mid1 protein in this organism. Here, we characterized the kinetic property of a putative Cch1–Mid1 Ca channel overexpressed in cells, and showed that the L-type VGCC blockers nifedipine and verapamil partially inhibited Cch1–Mid1 activity, but typical P/Q-, N-, R- and T-type VGCC blockers did not inhibit activity. In contrast, a third L-type VGCC blocker, diltiazem, increased Cch1–Mid1 activity. Diltiazem did not increase Ca uptake in the Δ and Δ single mutants and the Δ Δ double mutant, indicating that the diltiazem-induced increase in Ca uptake is completely dependent on Cch1–Mid1. These results suggest that Cch1 is pharmacologically similar to L-type VGCCs, but the interactions between Cch1 and the L-type VGCC blockers are more complicated than expected.

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2008-12-01
2020-04-07
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