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KCNK3 encodes a member of the superfamily of potassium channel proteins that contain two pore-forming P domains. Additionally we are shipping Potassium Channel, Subfamily K, Member 3 Antibodies (93) and many more products for this protein.
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A burden of rare variants in BMPR2 (show BMPR2 Proteins) significantly contributed to the risk of pulmonary arterial hypertension. In the remaining one family, the patient carried a pathogenic variant in a member of potassium channels, KCNK3, which was the first replicative finding of channelopathy in an Asian population.
The results suggested that heterodimerization of TASK1 and TALK2 provides cells with the ability to make multiple responses to a variety of physiological and pharmacological stimuli.
Genetic variation in the KCNK3 gene may contribute to Blood pressure variation and less severe Hypertensive disorders in which aldosterone may be one of several causative factors
Knockdown of TASK-1 by siRNA significantly enhanced apoptosis and reduced proliferation in Non-Small Cell Lung Cancer A549 cells, but not in weakly TASK-1 expressing NCI-H358 cells.
The present report supports the contribution of KCNK3 mutations to the genetic etiology of Pulmonary arterial hypertension and strongly suggests that mutations in KCNK3 follow incomplete dominance with worsening of the clinical features in homozygous patients.
In a cohort with idiopathic or hereditary pulmonary arterial hypertension, a possibly associated mutation was found in 11.10% of the idiopathic cases (n = 16) and in 68.18% of the hereditary cases. There were 3 mutations found in KCNK3.
Functional alanine-mutagenesis screens of TASK-1 and TRAAK (show KCNK4 Proteins) were used to build an in silico model of the TASK-1 cap.
control of TASK-1 trafficking by COPI, kinases, phosphatases and 14-3-3 (show YWHAQ Proteins) proteins is highly dynamic.
KCNK3 expression and function were reduced in pulmonary artery smooth muscle cells and endothelial cells in human pulmonary arterial hypertension.
TASK-1 and TASK-3 (show KCNK9 Proteins) may form heterodimers in human atrial cardiomyocytes.
While there is compelling evidence that TASK-1 is involved in the pathogenesis of pulmonary arterial hypertension in humans, the mouse does not appear to serve as a suitable model to study the underlying molecular mechanisms
the K(+) channel (show KCNC4 Proteins) TASK1 controls the thermogenic activity in brown adipocytes through modulation of beta-adrenergic receptor signaling.
KCNK3 channels are not involved in hearing.
An important role for TASK-1 channels in limiting pancreatic alpha-cell excitability and glucagon (show GCG Proteins) secretion during glucose stimulation.
A glucose-dependent role for beta-cell TASK-1 channels of limiting glucose-stimulated Deltapsip depolarization and insulin (show INS Proteins) secretion, which modulates glucose homeostasis.
Oxygen and mitochondrial inhibitors modulate both monomeric and heteromeric TASK-1 and TASK-3 (show KCNK9 Proteins) channels in mouse carotid body type-1 cells.
This study demonstrated for the first time that oligodendrocytes express functional TASK-1 channels and provide compelling evidence they contribute to oligodendrocyte damage in hypoxia.
TASK-1 deficiency does neither alter key electrophysiological parameters nor increases atrial/ventricular vulnerability after electrical stimulation.
The PCR data revealed the existence of two astrocytic subpopulations markedly differing in their gene expression levels for inwardly rectifying K+ channels (Kir4.1 (show KCNJ10 Proteins)), K(2P) channels (TREK-1 (show KCNK2 Proteins) and TWIK-1 (show KCNK1 Proteins)) and Cl- channels (ClC2 (show CLCN2 Proteins)).
No difference is found between the pulmonary artery (PA) of wild-type and TASK-1/3-deficient mice; TASK-1 does not form a functional channel in pulmonary artery smooth muscle cells.
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.
potassium channel subfamily K member 3
, TWIK-related acid-sensitive K(+) channel 1
, TWIK-related acid-sensitive K+ channel
, acid-sensitive potassium channel protein TASK
, acid-sensitive potassium channel protein TASK-1
, cardiac potassium channel
, potassium inwardly-rectifying channel, subfamily K, member 3
, two P domain potassium channel
, two pore K(+) channel KT3.1
, two pore potassium channel KT3.1
, cardiac two pore background K(+) channel
, TASK-1 potassium channel