Anti-slobeta3 (KCNMB3) (extracellular)

Antibodies

Israel

Storage before Reconstitution: The antibody ships as a lyophilized powder at room temperature. Upon arrival, it should be stored at -20°C - Storage after Reconstitution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods, small aliquots should be stored at -20°C. Avoid multiple freezing and thawing. Centrifuge all antibody preparations before use (10000 x g 5 min).

A Rabbit Polyclonal Antibody to sloβ3 (KCNMB3) Subunit

Polyclonal

Western blot analysis

50 µl or 0.2 ml double distilled water (DDW), depending on the sample size.

1% BSA, 0.05% NaN3

KCNMB3

Rat

41116161

Large-conductance, voltage- and Ca2+-activated K+ channels, also known as the BK channels, are widely expressed channels that couple changes in submembrane Ca2+ concentration to the regulation of electrical excitability1. BK channels are formed from four α-subunits arising from the Slowpoke (Slo) gene product2. In addition, in smooth muscle and cochlea, an accessory β-subunit can regulate BK channel gating profoundly. At present, four β subunits have been cloned in mammals. β subunits alter the Ca2+ sensitivity and gating kinetics of BK channels, greatly contributing to BK channel diversity. On the other hand, they modify the BK channel pharmacological properties, changing toxin binding and acting as receptors for drugs3.Regulatory β subunits share a putative membrane topology, with two transmembrane segments connected by a 120- residue extracellular loop and with NH2 and COOH terminals oriented toward the cytoplasm4. Each β subunit has a tissue-specific expression and modulates channel function uniquely which provides a major mechanism for diverse BK channel phenotypes in various tissues.β3 is highly expressed in kidney, heart, and brain5. The β3 gene (KCNMB3) associates with Slo1 α subunits and regulate BK channel function. In humans, the β3 gene contains four N-terminal alternative exons that produce four functionally distinct β3 subunits, β3a-d. Three variants, β3a-c, exhibit kinetically distinct inactivation behaviors6. A mutation in the β3 gene is linked to idiopathic epilepsy7.