SCUBA

KCNQ1 — Potassium voltage-gated channel subfamily Q member 1

KCNQ1 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

KCNQ1's module in each cell type

Cell typeModuleShares the module with
EnterocytesLong-gene intronic signal
Technical artifact
ASCC3, CASK, LGR4, MAP3K5, MECOM, MID1, PPP1R9A, RALGAPA2 +5 moreView in SCUBA
MacrophagesMacrophage Migration
Migration & adhesion
CEMIP2, CPM, EPB41L2, EPS8, GBE1, ITGA9, MAN1A1, MEF2C +12 moreView in SCUBA

About the gene

SynonymsJLNS1, KCNA8, KCNA9, Kv7.1, KVLQT1, LQT, LQT1
Chromosome11: 2444684-2849105
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classDisease related genes, FDA approved drug targets, Human disease related genes, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins, Transporters, Voltage-gated ion channels
Molecular functionCalmodulin-binding, Ion channel, Potassium channel, Voltage-gated channel
Biological processIon transport, Potassium transport, Transport

Function

Pore-forming subunit of the voltage-gated potassium (Kv) channel involved in the regulation of cardiomyocyte excitability and important in normal development and functions of myocardium, inner ear, stomach and colon. Associates with KCNE beta subunits that modulates current kinetics. Induces a voltage-dependent current by rapidly activating and slowly deactivating potassium-selective outward current. Also promotes 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). Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current. When associated with KCNE3, forms the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions. 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. When associated with KCNE4, inhibits voltage-gated potassium channel activity. When associated with KCNE5, this complex only conducts current upon strong and continued depolarization. Also forms a heterotetramer with KCNQ5; has a voltage-gated potassium channel activity. Binds with phosphatidylinositol 4,5-bisphosphate. KCNQ1-KCNE2 channel associates with Na(+)-coupled myo-inositol symporter in the apical membrane of choroid plexus epithelium and regulates the myo- inositol gradient between blood and cerebrospinal fluid with an impact on neuron excitability (By similarity). Non-functional alone but modulatory when coexpressed with the full-length isoform 1

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.