Biology:KCNMB1

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

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. "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. Aug 1996. doi:10.1073/pnas.93.17.9200. PMID 8799178. Bibcode1996PNAS...93.9200T. 
  2. "Human and rodent MaxiK channel beta-subunit genes: cloning and characterization". Genomics 55 (1): 57–67. Jan 1999. 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". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3779. 
  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. PMID 25015960. 

Further reading

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