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|
|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)|
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.
Fig.1 Regulation of TASK-1 in pulmonary artery smooth muscle cells. (Olschewski, 2017)
Application of KCNK3 Membrane Protein in Literature
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.
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.
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.
The expression and function of KCNK3 were decreased in pulmonary artery smooth muscle cells and human pulmonary arterial hypertension endothelial cells.
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
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