Target:MaxiKβ
Fields:cGMP-PKG signaling pathway;Vascular smooth muscle contraction;Insulin secretion
Gene Name:KCNMB4
Protein Name:Calcium-activated potassium channel subunit beta-4
Human Gene Id:27345
Human Swiss Prot No:Q86W47
Mouse Gene Id:58802
Mouse Swiss Prot No:Q9JIN6
Rat Gene Id:66016
Rat Swiss Prot No:Q9ESK8
Immunogen:The antiserum was produced against synthesized peptide derived from human MaxiKbeta. AA range:70-119
Specificity:MaxiKβ Polyclonal Antibody detects endogenous levels of MaxiKβ protein.
Formulation:Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source:Polyclonal, Rabbit,IgG
Dilution:WB 1:500 - 1:2000. IHC 1:100 - 1:300. ELISA: 1:20000.. IF 1:50-200
Purification:The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration:1 mg/ml
Storage Stability:-15°C to -25°C/1 year(Do not lower than -25°C)
Other Name:KCNMB4;Calcium-activated potassium channel subunit beta-4;BK channel subunit beta-4;BKbeta4;Hbeta4;Calcium-activated potassium channel; subfamily M subunit beta-4;Charybdotoxin receptor subunit beta-4;K(VCA)beta-4;Maxi K channel sub
Observed Band(KD):24kD
Background: 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 slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit. [provided by RefSeq, Jul 2008],
Function:domain:Resistance to charybdotoxin (CTX) toxin is mediated by the extracellular domain.,function:Regulatory subunit of the calcium activated potassium KCNMA1 (maxiK) channel. Modulates the calcium sensitivity and gating kinetics of KCNMA1, thereby contributing to KCNMA1 channel diversity. Decreases the gating kinetics and calcium sensitivity of the KCNMA1 channel, but with fast deactivation kinetics. May decrease KCNMA1 channel openings at low calcium concentrations but increases channel openings at high calcium concentrations. Makes KCNMA1 channel resistant to 100 nM charybdotoxin (CTX) toxin concentrations.,miscellaneous:Treatment with okadaic acid reduces its effect on KCNMA1.,PTM:N-glycosylated. A highly glycosylated form is promoted by KCNMA1. Glycosylation, which is not required for the interaction with KCNMA1 and subcellular location, increases protection against charybdotoxin.,PT
Subcellular Location:Membrane; Multi-pass membrane protein.
Expression:Predominantly expressed in brain. In brain, it is expressed in the cerebellum, cerebral cortex, medulla, spinal cord, occipital pole, frontal lobe, temporal lobe, putamen, amygdala, caudate nucleus, corpus callosum, hippocampus, substantia nigra and thalamus. Weakly or not expressed in other tissues.