KCNMB2 is encoded by the KCNMB2 gene which is located on 3q26.2-q27.1 in humans. And the molecular mass of KCNMB2 is about 27 kDa. KCNMB2 is highly expressed in the ovary, and it is found relatively high in kidney, heart and brain, but it’s expressed with low levels in other tissues. KCNMB2 belongs to the KCNMB subfamily. Structurally, KCNMB2 contains the ball and chain domain which mediates the interaction with KCNMA1. And the protein contains two transmembrane domains with intracellular N- and C-termini.
|Basic Information of KCNMB2|
|Protein Name||Calcium-activated potassium channel subunit beta-2|
|Aliases||BK channel subunit beta-2, BKbeta2, Hbeta2, Calcium-activated potassium channel, subfamily M subunit beta-2, Charybdotoxin receptor subunit beta-2, Hbeta3, K(VCA)beta-2, Maxi K channel subunit beta-2, Slo-beta-2|
|Organism||Homo sapiens (Human)|
|Transmembrane Times||Multi-pass membrane|
KCNMB2 is essentially a regulator subunit of KCNMA1, a calcium-activated potassium channel. Just like KCNMB1, KCNMB2 is also associated with the calcium sensitivity and gating kinetics of KCNMA1. In vivo, KCNMB2 can negatively regulate the activity of KCNMA1, rapidly and completely inactivating the KCNMA1 channel complex. The regulatory activity is mainly mediated by the N-termini. At the same time, KCNMB2 also participates in many other biological processes, for example, neuronal action potential, regulation of vasoconstriction and action potential. It has been revealed that KCNMB2 can limit KCNMA1 surface expression levels through the endocytic trafficking signals at the C-terminus, and coexpression with KCNMA1 causes a shift of KCNMA1’s cytoplasmic distribution. KCNMB2 knockdown mice excrete fewer K+ into the urine and display hyperaldosteronism, but they can achieve K+ balance through an aldosterone-mediated, KCNMB2-independent mechanism.
Fig.1 Ball-and-chain domains of KCNMB2. (Detlef l, 2001)
According to the previous finding that a paternal methyl donor-rich diet can negatively regulate expression of KCNMB, authors in this article explore the synaptic and intrinsic properties of CA1 pyramidal neurons of the F1 offspring mice, and they try to reveal the mechanisms of the phenomenon.
Accordingly, the physiological importance of KCNMB2 as an auxiliary subunit of large conductance Ca2+-activated K+ channel has not been revealed entirely. Authors in this article report that colonic K+ secretion is intact or even increased in KCNMB2 knockout mice.
It has been reported that KCNMB2 can influence the range of BK channel activation. In order to confirm this idea, authors in this article use KCNMB2 mice to test. They finally reveal that the idea is solid, at the same time, they find that the particular properties of BK channels in the absence of KCNMB2 perhaps predispose to burst firing.
This article reveals that KCNMB2 can negatively regulate the surface expression levels of KCNMA1 through an endocytic mechanism. The endocytic trafficking signals in C-terminus of KCNMB2 may function in the process.
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