KCNMB4 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
Aliases | KCNMB4 , potassium calcium-activated channel subfamily M regulatory beta subunit 4 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 605223 MGI: 1913272 HomoloGene: 8721 GeneCards: KCNMB4 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Calcium-activated potassium channel subunit beta-4 is a protein that in humans is encoded by the KCNMB4 gene. [5] [6] [7]
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 modulatory beta subunit. The protein encoded by this gene is an auxiliary beta subunit which slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit. [7]
Calcium-activated potassium channel subunit alpha-1 also known as large conductance calcium-activated potassium channel, subfamily M, alpha member 1 (KCa1.1), or BK channel alpha subunit, is a voltage gated potassium channel encoded by the KCNMA1 gene and characterized by their large conductance of potassium ions (K+) through cell membranes.
Guanine nucleotide-binding protein G(I)/G(S)/G(T) subunit beta-1 is a protein that in humans is encoded by the GNB1 gene.
Potassium voltage-gated channel subfamily D member 2 is a protein that in humans is encoded by the KCND2 gene. It contributes to the cardiac transient outward potassium current (Ito1), the main contributing current to the repolarizing phase 1 of the cardiac action potential.
Potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4, also known as KCNN4, is a human gene encoding the KCa3.1 protein.
Guanine nucleotide-binding protein G(I)/G(S)/G(O) subunit gamma-2 is a protein that in humans is encoded by the GNG2 gene.
Calcium-activated potassium channel subunit beta-1 is a protein that in humans is encoded by the KCNMB1 gene.
Chloride channel accessory 1 is a protein that in humans is encoded by the CLCA1 gene.
Voltage-dependent L-type calcium channel subunit beta-2 is a protein that in humans is encoded by the CACNB2 gene.
G protein-activated inward rectifier potassium channel 1(GIRK-1) is encoded in the human by the gene KCNJ3.
Voltage-dependent L-type calcium channel subunit beta-4 is a protein that in humans is encoded by the CACNB4 gene.
Voltage-gated potassium channel subunit beta-1 is a protein that in humans is encoded by the KCNAB1 gene.
Voltage-dependent L-type calcium channel subunit beta-3 is a protein that in humans is encoded by the CACNB3 gene.
Calcium-activated potassium channel subunit beta-2 is a protein that in humans is encoded by the KCNMB2 gene.
Calcium-activated potassium channel subunit beta-3 is a protein that in humans is encoded by the KCNMB3 gene.
Potassium intermediate/small conductance calcium-activated channel, subfamily N, member 2, also known as KCNN2, is a protein which in humans is encoded by the KCNN2 gene. KCNN2 is an ion channel protein also known as KCa2.2.
Voltage-dependent calcium channel subunit alpha-2/delta-1 is a protein that in humans is encoded by the CACNA2D1 gene.
Potassium voltage-gated channel subfamily KQT member 5 is a protein that in humans is encoded by the KCNQ5 gene.
Calcium channel, voltage-dependent, T type, alpha 1H subunit, also known as CACNA1H, is a protein which in humans is encoded by the CACNA1H gene.
Potassium voltage-gated channel subfamily G member 4 is a protein that in humans is encoded by the KCNG4 gene. The protein encoded by this gene is a voltage-gated potassium channel subunit.
Voltage-gated potassium channel subunit beta-3 is a protein that in humans is encoded by the KCNAB3 gene. The protein encoded by this gene is a voltage-gated potassium channel beta subunit.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.