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Reversibility of the Ca(2+) channel alpha(1)-beta subunit interaction

D Bichet1, C Lecomte, J M Sabatier

  • 1Laboratoire de Neurobiologie des Canaux Ioniques, Laboratoire de Biochimie, CNRS UMR 6560, INSERM U464, Institut Fédératif Jean Roche, Boulevard Pierre Dramard, Marseille Cedex 20, 13916, France.

Biochemical and Biophysical Research Communications
|November 4, 2000
PubMed

The auxiliary beta subunit importantly regulates voltage-dependent Ca(2+) channel activity through an interaction with the AID domain, a binding site located in the cytoplasmic I-II linker of the ion-conducting alpha(1) subunit. In the present study, we used two synthetic peptides corresponding to partial sequences of the I-II linker of alpha(1A) (AID(A)-peptides) as tools to disrupt the alpha(1)-beta interaction. In vitro binding experiments confirmed that these peptides exhibit a reasonable affinity to the neuronal beta(3) subunit to serve this purpose, although they failed to prevent immunoprecipitation of native N- and P/Q-type channels by anti-beta(3) antibodies. Together, our results (i) provide evidence for the reversibility of channel subunit association suggesting that the disruption of the alpha(1)-beta interaction may be a possible mechanism for Ca(2+) channel regulation in vivo, and (ii) support a model whereby the alpha(1)-beta association is based on multiple interaction sites.

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