Regulation of Ca-sensitive inactivation of a 1-type Ca2+ channel by specific domains of beta subunits.
Ca2+ channel auxiliary beta subunits have been shown to modulate voltage-dependent inactivation of various types of Ca2+ channels. The beta1 and beta2 subunits, that are differentially expressed with the L-type alpha1 Ca2+ channel subunit in heart, muscle and brain, can specifically modulate the Ca2+-dependent inactivation kinetics. Their expression in Xenopus oocytes with the alpha1C subunit leads, in both cases, to biphasic Ca2+ current decays, the second phase being markedly slowed by expression of the beta2 subunit. Using a series of beta subunit deletion mutants and chimeric constructs of beta1 and beta2 subunits, we show that the inhibitory site located on the amino-terminal region of the beta2a subunit is the major element of this regulation. These results thus suggest that different splice variants of the beta2 subunit can modulate, in a specific way, the Ca2+ entry through L-type Ca2+ channels in different brain or heart regions.
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CRBM, CNRS UPR 1086, IFR 24, Montpellier, France.
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D017398:Alternative Splicing; D000818:Animals; D001921:Brain / Q000378:metabolism; D002118:Calcium / Q000494:pharmacology*; D015220:Calcium Channels / Q000378:metabolism*; D020746:Calcium Channels, L-Type; D017931:DNA Primers / Q000235:genetics; D005786:Gene Expression Regulation; D009206:Myocardium / Q000378:metabolism; D009865:Oocytes / Q000378:metabolism; D018408:Patch-Clamp Techniques; D051381:Rats; D011994:Recombinant Proteins / Q000235:genetics; D017384:Sequence Deletion; D014981:Xenopus
D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D017931:DNA Primers; D011994:Recombinant Proteins; D002118:Calcium