Calcium-activated potassium channel subunit beta-3 is a protein that in humans is encoded by the KCNMB3gene.[4][5]
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 may partially inactivate or slightly decrease the activation time of MaxiK alpha subunit currents. At least four transcript variants encoding four different isoforms have been found for this gene.[5]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Riazi MA, Brinkman-Mills P, Johnson A, Naylor SL, Minoshima S, Shimizu N, Baldini A, McDermid HE (Feb 2000). "Identification of a putative regulatory subunit of a calcium-activated potassium channel in the dup(3q) syndrome region and a related sequence on 22q11.2". Genomics. 62 (1): 90–4. doi:10.1006/geno.1999.5975. PMID10585773.
Zeng XH, Xia XM, Lingle CJ (2003). "Redox-sensitive extracellular gates formed by auxiliary beta subunits of calcium-activated potassium channels". Nat. Struct. Biol. 10 (6): 448–54. doi:10.1038/nsb932. PMID12740608. S2CID19557594.
Hu S, Labuda MZ, Pandolfo M, et al. (2003). "Variants of the KCNMB3 regulatory subunit of maxi BK channels affect channel inactivation". Physiol. Genomics. 15 (3): 191–8. doi:10.1152/physiolgenomics.00110.2003. PMID14612589.
Lorenz S, Heils A, Kasper JM, Sander T (2007). "Allelic association of a truncation mutation of the KCNMB3 gene with idiopathic generalized epilepsy". Am. J. Med. Genet. B Neuropsychiatr. Genet. 144 (1): 10–3. doi:10.1002/ajmg.b.30369. PMID16958040. S2CID29047028.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.