Mutations of calcium channel beta subunit genes in mice

Ca2+ influx through high voltage activated Ca2+ channels initiates a number of physiological processes including e.g, excitation-contraction coupling in cardiac myocytes and excitation-transcription coupling in neurones. The Ca2+ channels involved are complexes of a pore-forming alpha(1) subunit, a transmembrane delta subunit disulfid-linked to an extracellular alpha(2) su bunit, a intracellular beta subunit and, at least in some tissues, a gamma subunit. Experimental analysis of beta subunit function comprises functiona l coexpression of its cDNA together with the cDNAs of the other subunits. T his experimental approach can be supplemented by investigating functional a lterations that result from the genetic elimination of Ca2+ channel beta ge nes in mice, Here we summarize the phenotype of mice deficient in the beta 1 subunit, the beta 3 subunit or the beta 4 subunit, respectively.