KCNMB1

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
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Calcium-activated potassium channel subunit beta-1 is a protein that in humans is encoded by the KCNMB1 gene.[1][2][3]

Function

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.[3] Beta subunits (beta 1-4) are highly tissue specific in their expression, with beta-1 being present predominantly on vascular smooth muscle. Endothelial cells are not known to express beta-1 subunits. Beta-1 is also known to be expressed in urinary bladder and in some regions of the brain. Association of the beta-1 subunit with the BK channel increases the apparent Ca2+ sensitivity of the channel and decreases voltage dependence.[4]

See also

References

  1. Tseng-Crank J, Godinot N, Johansen TE, Ahring PK, Strøbaek D, Mertz R, Foster CD, Olesen SP, Reinhart PH (Aug 1996). "Cloning, expression, and distribution of a Ca(2+)-activated K+ channel beta-subunit from human brain". Proceedings of the National Academy of Sciences of the United States of America. 93 (17): 9200–5. doi:10.1073/pnas.93.17.9200. PMC 38619. PMID 8799178.
  2. Jiang Z, Wallner M, Meera P, Toro L (Jan 1999). "Human and rodent MaxiK channel beta-subunit genes: cloning and characterization". Genomics. 55 (1): 57–67. doi:10.1006/geno.1998.5627. PMID 9888999.
  3. 3.0 3.1 "Entrez Gene: KCNMB1 potassium large conductance calcium-activated channel, subfamily M, beta member 1".
  4. Tano, J.-Y.; Gollasch, M. (2014). "Hypoxia and ischemia-reperfusion: a BiK contribution?". AJP: Heart and Circulatory Physiology. 307 (6): H811–H817. doi:10.1152/ajpheart.00319.2014. ISSN 0363-6135.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.



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