The smooth muscle-type β<sub>1</sub>subunit potentiates activation by DiBAC<sub>4</sub>(3) in recombinant BK channels

Calero, Cristina Bosch; Selga, Elisabet; Brugada, Ramón; Scornik, Fabiana S.; Pérez, Guillermo J.

doi:10.4161/chan.27212

Cited by 1 publication

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“…Moreover, β1 subunits promote a four-fold decrease in the K d of DiBAC 4 . Such findings could envision a new scope for the role β1 subunits in cardiovascular pharmacology (Bosch et al, 2014 ).…”

Section: The Role Of β Subunits In Bk Channel Pharmacologymentioning

confidence: 99%

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

2014

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Coded by a single gene (Slo1, KCM) and activated by depolarizing potentials and by a rise in intracellular Ca2+ concentration, the large conductance voltage- and Ca2+-activated K+ channel (BK) is unique among the superfamily of K+ channels. BK channels are tetramers characterized by a pore-forming α subunit containing seven transmembrane segments (instead of the six found in voltage-dependent K+ channels) and a large C terminus composed of two regulators of K+ conductance domains (RCK domains), where the Ca2+-binding sites reside. BK channels can be associated with accessory β subunits and, although different BK modulatory mechanisms have been described, greater interest has recently been placed on the role that the β subunits may play in the modulation of BK channel gating due to its physiological importance. Four β subunits have currently been identified (i.e., β1, β2, β3, and β4) and despite the fact that they all share the same topology, it has been shown that every β subunit has a specific tissue distribution and that they modify channel kinetics as well as their pharmacological properties and the apparent Ca2+ sensitivity of the α subunit in different ways. Additionally, different studies have shown that natural, endogenous, and synthetic compounds can modulate BK channels through β subunits. Considering the importance of these channels in different pathological conditions, such as hypertension and neurological disorders, this review focuses on the mechanisms by which these compounds modulate the biophysical properties of BK channels through the regulation of β subunits, as well as their potential therapeutic uses for diseases such as those mentioned above.

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Section: The Role Of β Subunits In Bk Channel Pharmacologymentioning

confidence: 99%

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

2014

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The smooth muscle-type β₁subunit potentiates activation by DiBAC₄(3) in recombinant BK channels

Abstract: 5 μM (α+β 1 ), and G-V curves shift up to −40mV and -110 mV, respectively. β 1 to β 2 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.

Cited by 1 publication

References 38 publications

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

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The smooth muscle-type β1subunit potentiates activation by DiBAC4(3) in recombinant BK channels

Abstract: 5 μM (α+β 1 ), and G-V curves shift up to −40mV and -110 mV, respectively. β 1 to β 2 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.

Cited by 1 publication

References 38 publications

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

Pharmacological consequences of the coexpression of BK channel Î± and auxiliary Î² subunits

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The smooth muscle-type β₁subunit potentiates activation by DiBAC₄(3) in recombinant BK channels