Description: potassium large conductance calcium-activated channel, subfamily M, beta member 1
Gene: Kcnmb1     Synonyms: SLO-BETA, hslo-beta, K(VCA)beta, KCNMB1

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BK channels are broadly expressed, and have functional roles in vascular smooth muscle as well as other tissues including skeletal muscle, neurons, kidney and secretory cells (Sah [1171], Vergara [1100], Kaczorowski [1172]). The functional diversity required for the tissue-specific roles of BK channels may be created in part by association with accessory b-subunits. A family of four BK b-subunits has been identified (Brenner [1169], Behrens [1173]). Each family member has a different tissue distribution and different effects on BK channel pharmacology and activation gating. The b1-subunit is enriched in smooth muscle and purifies with the BK pore-forming subunit (knaus [1172]). In expression systems, the b1 subunit confers an increased calcium sensitivity, slows gating kinetics and increases the sensitivity to the agonist dehydrosoyasaponin (DHS-1) (McManus [1163]).

KCNMB1 (also known as SLO-BETA; hslo-beta; K(VCA)beta) encodes the BkB1 channel. MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit and the product of this gene, the modulatory beta subunit. Intracellular calcium regulates the physical association between the alpha and beta subunits.



RGD ID Chromosome Position Species
2961 10 18904902-18912604 Rat
736975 11 33863013-33873638 Mouse
733456 5 169805167-169816638 Human

Kcnmb1 : potassium large conductance calcium-activated channel, subfamily M, beta member 1



Acc No Sequence Length Source
NM_019273 n/A n/A NCBI
NM_031169 n/A n/A NCBI
NM_004137 n/A n/A NCBI



Accession Name Definition Evidence
GO:0008076 voltage-gated potassium channel complex A protein complex that forms a transmembrane channel through which potassium ions may cross a cell membrane in response to changes in membrane potential. IEA
GO:0016020 membrane Double layer of lipid molecules that encloses all cells, and, in eukaryotes, many organelles; may be a single or double lipid bilayer; also includes associated proteins. IEA
GO:0016021 integral to membrane Penetrating at least one phospholipid bilayer of a membrane. May also refer to the state of being buried in the bilayer with no exposure outside the bilayer. When used to describe a protein, indicates that all or part of the peptide sequence is embedded in the membrane. IEA





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At the molecular level, the BK channel in vascular smooth muscle is formed by an ion-conducting α subunit (Meera [1164]) and a regulatory β1 subunit, encoded by KCNMB1 (McManus [1162], Tanaka [1163], Orio [540]).





Using sensitivity to DHS-1 as a probe for BK a/b1 subunits, it has been shown that human coronary artery smooth muscle is enriched for a/b1-assembled BK channels, and that these channels are more calcium sensitive than BK channels in other tissues where the b1 subunit is not expressed. (Tanaka [1163])

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The control of arterial tone depends on a calcium signal in the vascular smooth muscle, mainly provided by the influx of Ca2+ via voltage-gated channels and its release from intracellular stores (Jaggar [1165]). A key element in the control of the vascular tone is the large-conductance, Ca2+- and voltage-dependent K+ (BK) channel, which couples local increases in intracellular Ca2+ to aug- mented channel activity and vascular relaxation (Jaggar [1165], Toro [1166]). In smooth muscle, an increase in BK channel activity is induced by local releases of Ca2+ from the sarcoplasmic reticulum (“Ca2+ sparks”) that lead to hyperpolarization of the membrane and prevention of further influx of Ca2+ (Jaggar [1165]). This negative-feedback mechanism is finely tuned by the presence of the β1 subunit of the BK channel, which increases channel sensitivity to Ca2+ (McManus [1162], Orio [540], Knaus [1167], Meera [1168], Brenner [1169], Pluger [1170]).

KCNMB1 gene might be involved in the pathogenesis of human hypertension. (Fernandez-Fernandez [243])

Targeted deletion of the gene for the b1 subunit leads to a decrease in the calcium sensitivity of BK channels, a reduction in functional coupling of calcium sparks to BK channel activation, and increases in arterial tone and blood pressure. The b1 subunit of the BK channel, by tuning the channel's calcium sensitivity, is a key molecular component in translating calcium signals to the central physiological function of vasoregulation. (Brenner [1169])







Orio P et al. New disguises for an old channel: MaxiK channel beta-subunits.
News Physiol. Sci., 2002 Aug , 17 (156-61).

Jaggar JH et al. Calcium sparks in smooth muscle.
Am. J. Physiol., Cell Physiol., 2000 Feb , 278 (C235-56).

Toro L et al. Maxi-K(Ca), a Unique Member of the Voltage-Gated K Channel Superfamily.
News Physiol. Sci., 1998 Jun , 13 (112-117).

Vergara C et al. Calcium-activated potassium channels.
Curr. Opin. Neurobiol., 1998 Jun , 8 (321-9).

Kaczorowski GJ et al. High-conductance calcium-activated potassium channels; structure, pharmacology, and function.
J. Bioenerg. Biomembr., 1996 Jun , 28 (255-67).



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