title: Mutations of calcium channel beta subunit genes in mice.
abstract: 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 alpha1 subunit, a transmembrane delta subunit disulfide-linked to an extracellular alpha2 subunit, a intracellular beta subunit and, at least in some tissues, a gamma subunit. Experimental analysis of beta subunit function comprises functional coexpression of its cDNA together with the cDNAs of the other subunits. This experimental approach can be supplemented by investigating functional alterations that result from the genetic elimination of Ca2+ channel beta genes in mice. Here we summarize the phenotype of mice deficient in the beta1 subunit, the beta3 subunit or the beta4 subunit, respectively.
authors.affiliation: Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Freise
authors.forename: N
authors.initials: N
authors.lastname: Himmerkus
authors.forename: G
authors.initials: G
authors.lastname: Schroth
authors.forename: C
authors.initials: C
authors.lastname: Trost
authors.forename: P
authors.initials: P
authors.lastname: Weissgerber
authors.forename: M
authors.initials: M
authors.lastname: Freichel
authors.forename: V
authors.initials: V
authors.lastname: Flockerzi
mesh_terms: D000818:Animals; D015220:Calcium Channels / Q000235:genetics*; D051379:Mice; D009154:Mutation
chemical_list: D015220:Calcium Channels