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Calcium-activated potassium channel subunit beta-3 (KCNMB3)

Target
KCNMB3
Molecular classification
Ion channel (regulatory subunit), Calcium-activated potassium channel auxiliary subunit
01

Overview

Calcium-activated potassium channel subunit beta-3 (KCNMB3) is an auxiliary regulatory subunit of the large conductance, voltage, and calcium-sensitive potassium (BK, MaxiK) channels. It modulates the channel's calcium sensitivity and gating kinetics by associating with the pore-forming alpha subunit KCNMA1, thus contributing to functional diversity. Different isoforms of KCNMB3 can partially inactivate or slightly alter the activation kinetics of the BK channel current, and at least two subunits are required to exert inactivation effects. MaxiK channels, regulated by KCNMB3, are fundamental for the control of smooth muscle tone and neuronal excitability, linking intracellular Ca2+ increases to membrane potential changes. Mutations in KCNMB3 have been implicated in neurological and retinal disorders[1][3][5].

Other names
Potassium calcium-activated channel subfamily M regulatory beta subunit 3Potassium large conductance calcium-activated channel, subfamily M beta member 3Calcium-activated potassium channel, subfamily M subunit beta-3BK channel subunit beta-3BKbeta3Maxi K channel subunit beta-3Slo-beta-3Charybdotoxin receptor subunit beta-3K(VCA)beta-3KCNMB2KCNMBLMaxiK channel beta-subunit 3BK channel beta subunit 3Big potassium channel beta subunit 3HBETA3SLOBETA3
02

Mechanism of action

Channel activation (by increasing calcium sensitivity or channel open probability); Channel inhibition/blockade (by reducing channel function or altering gating kinetics); Modulation of inactivation kinetics in co-assembly with the pore-forming alpha subunit (KCNMA1)

03

Biological functions

Regulation of potassium channel activityModulation of neuronal excitabilityControl of smooth muscle toneCoupling intracellular calcium signals to membrane potential
04

Disease associations

Neurological disease (e.g., Paroxysmal Nonkinesigenic Dyskinesia 3)Retinal disease (e.g., Retinitis pigmentosa 51)Potential involvement in cardiovascular disease (smooth muscle regulation)
05

Safety considerations

CNS side effects due to altered neuronal excitability (inhibition/activation in the brain)Cardiac or vascular effects through dysregulation of smooth muscle toneLimited selectivity and potential off-target effects with available modulators
06

Interacting drugs

Colforsin (activator)

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