Anti-KCNQ1 K+ Channel Antibody (11510)

Fusion protein aa 2-101 of human KCNQ1 (K+7.1, KvLQT1, accession number P51787).

PBS, pH 7.4, 50% glycerol, 0.09% sodium azide.

Liquid

Purified by Protein G affinity chromatography

This antibody is stable for at least one (1) year at -20°C. Avoid repeated freeze-thaw cycles.

For in vitro investigational use only. Not for use in therapeutic or diagnostic procedures.

Next Day 2-8°C

This antibody recognizes human, mouse and rat KCNQ1.

Ion channels are integral membrane proteins that help establish and control the small voltage gradient across the plasma membrane of living cells by allowing the flow of ions down their electrochemical gradient. –+7.1 (KvLQT1) is a potassium channel protein coded for by the gene KCNQ1. K+7.1 is present in cell membranes of cardiac muscle tissue and in inner ear neurons among other tissues. In cardiac cells, K+7.1 mediates the I. (or slow delayed rectifying K3) current that contributes to repolarization of the cell, terminating the cardiac potential and, thereby, the heart's contractions.

Potassium channel that plays an important role in a number of tissues, including heart, inner ear, stomach and colon (PubMed:10646604, PubMed:25441029). Associates with KCNE beta subunits that modulates current kinetics (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505, PubMed:19687231). Induces a voltage-dependent current by rapidly activating and slowly deactivating potassium-selective outward current (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505, PubMed:25441029). Promotes also a delayed voltage activated potassium current showing outward rectification characteristic (By similarity). During beta-adrenergic receptor stimulation participates in cardiac repolarization by associating with KCNE1 to form the I(Ks) cardiac potassium current that increases the amplitude and slows down the activation kinetics of outward potassium current I(Ks) (By similarity) (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505). Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current (PubMed:10713961). When associated with KCNE3, forms the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions (PubMed:10646604). This interaction with KCNE3 is reduced by 17beta-estradiol, resulting in the reduction of currents (By similarity). During conditions of increased substrate load, maintains the driving force for proximal tubular and intestinal sodium ions absorption, gastric acid secretion, and cAMP-induced jejunal chloride ions secretion (By similarity). Allows the provision of potassium ions to the luminal membrane of the secretory canaliculus in the resting state as well as during stimulated acid secretion (By similarity). When associated with KCNE2, forms a heterooligomer complex leading to currents with an apparently instantaneous activation, a rapid deactivation process and a linear current-voltage relationship and decreases the amplitude of the outward current (PubMed:11101505). When associated with KCNE4, inhibits voltage-gated potassium channel activity (PubMed:19687231). When associated with KCNE5, this complex only conducts current upon strong and continued depolarization (PubMed:12324418). Also forms a heterotetramer with KCNQ5; has a voltage-gated potassium channel activity (PubMed:24855057). Binds with phosphatidylinositol 4,5-bisphosphate (PubMed:25037568). {UniProtKB:P97414, UniProtKB:Q9Z0N7, PubMed:10646604, PubMed:10713961, PubMed:11101505, PubMed:12324418, PubMed:19687231, PubMed:24855057, PubMed:25037568, PubMed:8900283, PubMed:9108097, PubMed:9312006}.; [Isoform 2]: Non-functional alone but modulatory when coexpressed with the full-length isoform 1. {PubMed:9305853}.