ArticleChannels (Austin, Tex.)2014
The smooth muscle-type β1 subunit potentiates activation by DiBAC4(3) in recombinant BK channels.
Article in Channels (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Pharmacological consequences of the coexpression of BK channel α and auxiliary β subunits.Frontiers in physiology · 2014Review
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Authors and funding
5 authors.
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Abstract
Large-conductance Ca(2+)-activated (BK) channels, expressed in a variety of tissues, play a fundamental role in regulating and maintaining arterial tone. We recently demonstrated that the slow voltage indicator DiBAC4(3) does not depend, as initially proposed, on the β 1 or β 4 subunits to activate native arterial smooth muscle BK channels. Using recombinant mslo BK channels, we now show that the β 1 subunit is not essential to this activation but exerts a large potentiating effect. DiBAC4(3) promotes concentration-dependent activation of BK channels and slows deactivation kinetics, changes that are independent of Ca(2+). Kd values for BK channel activation by DiBAC4(3) in 0 mM Ca(2+) are approximately 20 μM (α) and 5 μM (α+β 1), and G-V curves shift up to -40 mV and -110 mV, respectively. β1 to β2 mutations R11A and C18E do not interfere with the potentiating effect of the subunit. Our findings should help refine the role of the β 1 subunit in cardiovascular pharmacology.
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