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
Cat:
SL7689R
Species Reactivity:
Rat,(predicted: Human,Mouse,Pig,Cow,Horse,Sheep,)
Immunogen:
KLH conjugated synthetic peptide derived from human KCNMB1:10-80/191<Extracellular>
Format:
Liquid
Storage instructions:
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Concentration:
1mg/ml
Clonality:
Polyclonal
Isotype:
IgG
Applications:
ELISA=1:5000-10000IHC-P=1:100-500IHC-F=1:100-500IF=1:100-500(Paraffin sections need to do antigen repair)not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.
Potassium channels are a group of ubiquitously expressed proteins that serve numerous functions in excitable and non-excitable cells. One class of integral membrane potassium channels is the large conductance, calcium-activated potassium channel (Maxi K+). Maxi K+ differs from most other potassium channels in that its activation is controlled by both increases in intracellular calcium and by membrane depolarization. Maxi K+ dual activation is possible because of its structure. The core of the channel, which is similar to other potassium channels, is a Maxi K+ alpha homotetramer that contains both a voltage sensor and an intracellular calcium binding domain. In vascular smooth muscle, an auxiliary beta-subunit is found in a 1:1 stoichiometry. The beta-subunit exhibits its effect on the Maxi K+ channel by effectively decreasing by 5- to 10- fold the concentration of calcium required to keep the pore open. Maxi K+ beta is the target for possible therapeutics because of its role in blood flow and blood pressure regulation.
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. Increases the apparent Ca(2+)/voltage sensitivity of the KCNMA1 channel. It also modifies KCNMA1 channel kinetics and alters its pharmacological properties. It slows down the activation and the deactivation kinetics of the channel. Acts as a negative regulator of smooth muscle contraction by enhancing the calcium sensitivity to KCNMA1. Its presence is also a requirement for internal binding of the KCNMA1 channel opener dehydrosoyasaponin I (DHS-1) triterpene glycoside and for external binding of the agonist hormone 17-beta-estradiol (E2). Increases the binding activity of charybdotoxin (CTX) toxin to KCNMA1 peptide blocker by increasing the CTX association rate and decreasing the dissociation rate.
Subunit: Interacts with KCNMA1 tetramer. There are probably 4 molecules of KCMNB1 per KCNMA1 tetramer.
Tissue Specificity: Abundantly expressed in smooth muscle. Low levels of expression in most other tissues. Within the brain, relatively high levels found in hippocampus and corpus callosum.
Post-translational modifications: N-glycosylated.
Similarity: Belongs to the KCNMB (TC 8.A.14.1) family. KCNMB1 subfamily.
Specific References (1) | SL7689R has been referenced in 1 publications.
[IF=2.447] Yiyuan Zhou. et al. Fumaric acid and succinic acid treat gestational hypertension by downregulating the expression of KCNMB1 and TET1. Exp Ther Med. 2021 Oct;22(4):1-7 IHC ; Rat.