KCNK3 Membrane Protein Introduction

Introduction of KCNK3

KCNK3, the full name is potassium channel subfamily K member 3, also known as acid-sensitive potassium channel protein TASK-1, TWIK-related acid-sensitive K(+) channel 1, two-pore potassium channel KT3.1. KCNK3 belongs to the two-pore domain potassium channel family. This subfamily of genes has constitutive activity at physiological resting membrane potentials in excitable cells, including smooth muscle cells, and is particularly associated with human pulmonary circulation. KCNK3 showed approximately half of the maximum activity at physiological extracellular pH (7.4). It can be effectively inhibited or activated by acidosis or alkalosis, respectively. KCNK3 often forms a heterodimer with TASK-3. They are thought to contribute to background currents in many neuronal populations throughout the central nervous system, including cerebellar granule neurons, cerebral cortex, brainstem Pre-Botzinger and retrotrapezoid regions, hippocampal neurons, thalamic relay neurons, hypoglossal nerves, and spinal motor neurons, dorsal vagus neurons. In peripheral tissues, high levels of KCNK3 expression have been found in the carotid body, in the atrium of the heart and in neuroepithelial of the lung.

Basic Information of KCNK3
Protein Name Potassium channel subfamily K member 3
Gene Name KCNK3
Aliases Acid-sensitive potassium channel protein TASK-1, TWIK-related acid-sensitive K(+) channel 1, two-pore potassium channel KT3.1 (two-pore K(+) channel KT3.1)
Organism Homo sapiens (Human)
UniProt ID O14649
Transmembrane Times 4
Length (aa) 394

Function of KCNK3 Membrane Protein

KCNK3 channels are sensitive to a variety of physiological and pharmacological mediators that affect their activity, such as unsaturated fatty acids, extracellular pH, hypoxia, anesthetics, and intracellular signaling pathways. Direct or indirect regulation of the KCNK3 channel by targeting its regulatory mechanisms has the potential to control human pulmonary artery tone. In addition, KCNK3 mutations have been identified as a rare cause of both familial and idiopathic pulmonary arterial hypertension. Peripheral chemoreceptor glomus cells in the carotid body express heterodimers composed of KCNK3 and TASK-3 in their plasma membrane, and their inhibition of background K+ current and the following depolarization in response to acidification contributes to increased ventilation.

Regulation of TASK-1 in pulmonary artery smooth muscle cells. Fig.1 Regulation of TASK-1 in pulmonary artery smooth muscle cells. (Olschewski, 2017)

Application of KCNK3 Membrane Protein in Literature

  1. Suzuki Y., et al. Heterodimerization of two pore domain K+ channel TASK1 and TALK2 in living heterologous expression systems. PLoS One. 2017, 12(10):e0186252. PubMed ID: 29016681

    The results indicated that heterodimerization of TASK1 and TALK2 conferred the ability of cells to produce multiple responses to a variety of physiological and pharmacological stimuli.

  2. Huertas A., et al. New targets for pulmonary arterial hypertension: going beyond the currently targeted three pathways. Curr Opin Pulm Med. 2017, 23(5):377-385. PubMed ID: 28582316

    A familial case of pulmonary arterial hypertension associated with heterozygous missense variation in the KCNK3 gene (coding the two-hole domain potassium channel TASK-1) had been described as having a prevalence of 1.3% and 3.2% in idiopathic pulmonary arterial hypertension and hereditary pulmonary arterial hypertension, respectively.

  3. Manichaikul A., et al. KCNK3 Variants Are Associated with Hyperaldosteronism and Hypertension. Hypertension. 2016, 68(2):356-64. PubMed ID: 27296998

    Genetic variation of the KCNK3 gene might lead to blood pressure variability and less severe hypertension, in which aldosterone might be one of several pathogenic factors.

  4. Antigny F., et al. Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension. Circulation. 2016, 133(14):1371-85. PubMed ID: 26912814

    The expression and function of KCNK3 were decreased in pulmonary artery smooth muscle cells and human pulmonary arterial hypertension endothelial cells.

  5. Dadi P.K., et al. Pancreatic β-cell-specific ablation of TASK-1 channels augments glucose-stimulated calcium entry and insulin secretion, improving glucose tolerance. Endocrinology. 2014, 155(10):3757-68. PubMed ID: 24932805

    The glucose-dependent role of the beta cell TASK-1 channel limited glucose-stimulated Deltaspip depolarization and insulin secretion, which regulated glucose homeostasis.

KCNK3 Preparation Options

Membrane protein studies have advanced significantly over the past few years. Based on our versatile Magic™ membrane protein production platform, we could offer a series of membrane protein preparation services for worldwide customers in reconstitution forms or other protein forms in the same family. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-KCNK3 antibody development services.

During the past years, Creative Biolabs has successfully generated many functional membrane proteins for our global customers. We are happy to accelerate the development of our clients’ programs with our one-stop, custom-oriented service. For more detailed information, please feel free to contact us.


  1. Olschewski A, et al. (2017). TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications. Eur Respir J. 50(5).

All listed customized services & products are for research use only, not intended for pharmaceutical, diagnostic, therapeutic or any in vivo human use.

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