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Properties of the α1-β Anchoring Site in Voltage-dependent Ca2+ Channels
Journal article   Open access   Peer reviewed

Properties of the α1-β Anchoring Site in Voltage-dependent Ca2+ Channels

Michel De Waard, Derrick R Witcher, Marlon Pragnell, Hongyan Liu and Kevin P Campbell
The Journal of biological chemistry, Vol.270(20), pp.12056-12064
05/19/1995
DOI: 10.1074/jbc.270.20.12056
PMID: 7744854
url
https://doi.org/10.1074/jbc.270.20.12056View
Published (Version of record) Open Access

Abstract

In voltage-dependent Ca2+ channels, the β subunit interacts with the α1 subunit via a cytoplasmic site. A biochemical assay has been developed to quantitatively describe the interaction between both subunits. In vitro synthesized35S-labeled β subunits specifically bind to a glutathione S -transferase (GST) fusion protein containing the α1ainteraction domain (AIDA, located between the amino-acids 383 and 400 of the cytoplasmic loop between the hydrophobic domains I and II). Kinetic analysis demonstrates that the association of35S-labeled β1bsubunit to the AIDAGST fusion protein occurs with a fast rate constant at 4°C. The binding is almost irreversible as demonstrated by the absence of dissociation observed after an 8-h incubation with an 18-amino acid synthetic AIDApeptide. The α1-β binding site does not seem to be a target for cytoplasmic regulation. The interaction is mostly unaffected by changes in ionic strength, pH, and Ca2+concentration or by protein kinase C phosphorylation. The specificity of subunit interaction in voltage-dependent Ca2+channels was also followed by saturation analyses. The data obtained show that the AIDAGST fusion protein binds to a single site on the β1bwith an apparent Kdof 5 nM. The affinities of AIDAGST fusion protein for various β subunits was measured and demonstrate that β subunits associate with different affinities to each α1interaction domain. The rank order of AIDAaffinity for each β subunit is as follows: β> > β> > β1b»β3. The binding of the β subunit to α1subunit can be inhibited in vitro by the AIDAsynthetic peptide with an apparent Kiof 285 nM. This interaction can also be prevented in heterologous Ca2+channels by the injection of the AIDAGST fusion protein into Xenopus oocytes. Our results demonstrate that the site of interaction between AID and β subunit is responsible for anchoring the β subunit to the α1subunit and thus allowing the β subunit to modify Ca2+channel activity.

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