KCNK3

Official Full Name

potassium two pore domain channel subfamily K member 3

Organism

Homo sapiens

Gene ID

3777

Background

This gene encodes a member of the superfamily of potassium channel proteins that contain two pore-forming P domains. The encoded protein is an outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane. Although three transcripts are detected in northern blots, there is currently no sequence available to confirm transcript variants for this gene. [provided by RefSeq, Aug 2008]

Synonyms

OAT1; PPH4; TASK; TASK1; TBAK1; K2p3.1; TASK-1

Cat.No.	Product Name	Price
CSC-DC007984	Panoply™ Human KCNK3 Knockdown Stable Cell Line	Inquiry
CSC-SC007984	Panoply™ Human KCNK3 Over-expressing Stable Cell Line	Inquiry

Cat.No.	Product Name	Price
AD08441Z	Human KCNK3 adenoviral particles	Inquiry
LV16016L	human KCNK3 (NM_002246) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHH323459	shRNA set against Human KCNK3 (NM_002246.2)	Inquiry
SHH323463	shRNA set against Mouse KCNK3 (NM_010608.2)	Inquiry
SHH323467	shRNA set against Rat KCNK3 (NM_033376.1)	Inquiry
SHL190452	shRNA set against Mouse Kcnk3(NM_010608.2)	Inquiry
SHL190506	shRNA set against Rat Kcnk3(NM_033376.1)	Inquiry

Cat.No.	Product Name	Price
CDFL006463	Mouse Kcnk3 cDNA Clone(NM_010608.2)	Inquiry
CDFR013019	Rat Kcnk3 cDNA Clone(NM_033376.1)	Inquiry
MiUTR1M-06250	KCNK3 miRNA 3'UTR clone	Inquiry
MiUTR1R-02832	KCNK3 miRNA 3'UTR clone	Inquiry
MiUTR4H-TG04708	KCNK3 miRNA 3'UTR clone	Inquiry
CDCB195488	Rabbit KCNK3 ORF clone (XM_008254648.1)	Inquiry
CDCG010743	Human KCNK3 ORF clone(NM_002246.2)	Inquiry
CDCL123193	Human Kcnk3 ORF clone (NM_010608.2)	Inquiry
CDCR380066	Rat Kcnk3 ORF Clone(NM_033376.1)	Inquiry

Detailed Information

Recent Research

KCNK3 is also called Twik-related acid-sensitive K⁺ channel (TASK1). The KCNK3 gene encodes for an outward K⁺ channel characterized by the presence of 4 transmembrane domains and 2 pore domains per subunit and is a member of 2-pore- domain K⁺ channels (K2P). It shares several characteristics with the background K⁺ current, including minimal voltage sensitivity, extracellular pH sensitivity, resistance to classic K⁺ channel inhibitors, and insensitivity to cytoplasmic Ca²⁺. This gene subfamily isconstitutively active at physiological resting membrane potentials in excitable cells, including smooth muscle cells, and has been particularly linked to the human pulmonary circulation. KCNK3 is sensitive to a wide array of physiological and pharmacological mediators that affect their activity such as unsaturated fatty acids, extracellular pH, hypoxia, anaesthetics and intracellular signalling pathways. Recent studies show that modulation of KCNK3, either directly or indirectly by targeting its regulatory mechanisms, has the potential to control pulmonary arterial tone in humans.

KCNK3 is highly expressed in human atrial cardiac myocytes and adrenal glomerulosa cells. Up-regulation of KCNK3 was reported in patients with chronic atrial fibrillation. Moreover,loss-of-function mutations in KCNK3 were also found to be associated with atrial fibrillation.Human KCNK3 variants are associated with hypertension and high plasma aldosterone levels. In addition, knockout mice lacking KCNK3 ischaracterised by impaired carotid body chemoreceptor function.

Pulmonary arterial hypertension (PAH) is a severe cardiopulmonary condition leading to right-sided heart failure and ultimately death. PAH caused by a KCNK3 mutation is an autosomal-dominant disease with incomplete penetrance. Recently, the identification of loss-of-function mutations in KCNK3 in some patients with PAH has highlighted a novel dysfunctional pathway and a potential therapeutic target. In addition, it has been demonstrated that loss of function of KCNK3 is a hallmark of idiopathic and heritable PAH and experimental pulmonary hypertension.

KCNK3 antagonizes norepinephrine-induced membrane depolarization by promoting potassium efflux in brown adipocytes. This limits calcium influx through voltage-dependent calcium channels and dampens adrenergic signaling, thereby attenuating lipolysis and thermogenic respiration. Adipose-specific KCNK3 knockout mice display increased energy expenditure and are resistant to hypothermia and obesity. These findings uncover a critical K⁺-Ca²⁺-adrenergic signaling axis that actstodampen thermogenesis, maintain tissue homeostasis, and reveal an electrophysiological regulatory mechanism of adipocyte function.

References:

Higasa K, et al. A burden of rare variants in BMPR2 and KCNK3 contributes to a risk of familial pulmonary arterial hypertension. BMC Pulmonary Medicine, 2017, 17(1).
Antigny F, et al. Potassium-Channel Subfamily K-Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension. Circulation, 2016, 8(3):247-248.
Olschewski A, et al. TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications. European Respiratory Journal, 2017, 50(5):1700754.

Quick Inquiry

KCNK3

You might be looking for:

Detailed Information