During the past decade a great number of genes encoding high- and low-voIta
ge-dependent Ca2+ channels and their accessory subunits have been cloned. S
tudies of Ca2+ channel structure-function relationships and channel regulat
ion using cDNA expression in heterologous expression systems have revealed
intricate details of subunit interaction, regulation of channels by protein
kinase A (PKA) and protein kinase C (PKC), drug binding sites, mechanisms
of drug action, the ion conduction pathway and other aspects of channel fun
ction. In recent years, however, we have arrived at the brink of an entirel
y new strategy to study Ca2+ channels by overexpressing or knocking out gen
es encoding these channels in transgenic mice. In this article, various mod
els of gene knockout or gene overexpression will be discussed. This new app
roach will reveal many secrets regarding Ca2+ channel regulation and the co
ntrol of Ca2+-dependent cellular processes.