Reactive species
Human;Mouse;Rat
Antibody type
Polyclonal Antibody
Protein name
Potassium voltage-gated channel subfamily E member 3 (MinK-related peptide 2) (Minimum potassium ion channel-related peptide 2) (Potassium channel subunit beta MiRP2)
Immunogen
Synthesized peptide derived from human protein . at AA range: 30-110
Specificity
KCNE3 Polyclonal Antibody detects endogenous levels of protein.
Constitute
Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB 1:500-2000 ELISA 1:5000-20000
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Background
potassium voltage-gated channel subfamily E regulatory subunit 3(KCNE3) Homo sapiens Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage-gated, isk-related subfamily. This member is a type I membrane protein, and a beta subunit that assembles with a potassium channel alpha-subunit to modulate the gating kinetics and enhance stability of the multimeric complex. This gene is prominently expressed in the kidney. A missense mutation in this gene is associated with hypokalemic periodic paralysis. [provided by RefSeq, Jul 2008],
Function
disease:Defects in KCNE3 are a cause of periodic paralysis hypokalemic (HOKPP) [MIM:170400]; also designated HYPOPP. HOKPP is an autosomal dominant disorder manifested by episodic flaccid generalized muscle weakness associated with falls of serum potassium levels.,disease:Defects in KCNE3 are a cause of thyrotoxic hypokalemic periodic paralysis (TPP) [MIM:188580]. TPP is seen in individuals of all races and manifests as attacks of episodic weakness with hypokalemia during thyrotoxicosis. TPP is seen most commonly in young Latin American or Asian men where up to 10% of thyrotoxic patients may have periodic paralysis. In such patients thyrotoxicosis has often been overlooked for many months. TPP generally occurs as a sporadic disease, and the periodic paralysis resolves completely with treatment of the thyrotoxicosis, although the muscle phenotype returns if the patient becomes thyrotoxic
