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mutations in the promoter region of the TWIK-related acid-sensitive K(+) channel 2 (TASK-2) gene did not result in hypertension or primary aldosteronism (PA) during long-term follow-up in healthy participants thus they do not seem to be a factor in causing PA by themselves.
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As a novel finding, our study suggests a role for KCNK5 in the regulation of platelet size and maturity. Furthermore, our findings confirm an association between the SH2B3-locus and platelet count.
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In human aldosterone-producing adrenocortical cancer cell lines, roxithromycin inhibited KCNJ5MUT-induced induction of CYP11B2 (encoding aldosterone synthase) expression and aldosterone production.
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HLA-DQB1*06:02 does not seem to be associated with hypoxic ventilatory response or hypercapnic ventilatory response; however there are point wise, uncorrected significant associations between two TASK2/KCNK5 variants (rs2815118 and rs150380866) and hypercapnic ventilatory response
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These results therefore provide further structural and functional insights into the possible pathophysiological effects of this missense variant in TASK-2.
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Results show that up-regulated KCNK5 in activated human T cells does not play a volume regulatory role, due to decreased Cl- permeability suggesting that the KCNK5 upregulation might play a role in hyperpolarization of the cell membrane leading to increased Ca2+ influx and proliferation of T cells.
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Potassium channel TASK2 drives human NK-cell proliferation and cytolytic function.
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Mutant genes (CELA1, HSPG2, and KCNK5) in Balkan endemic nephropathy patients encode proteins involved in basement membrane/extracellular matrix and vascular tone, tightly connected to process of angiogenesis.
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The TASK-2 channel lower expression represents a hallmark of aldosterone-producing adenoma causing aldosteronism and is associated with a higher expression of hsa-miR-23 and hsa-miR-34.
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Potassium channels, in particular K2P channels, are expressed and functional in the apical membrane of airway epithelial cells
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Disease activity in rheumatoid arthritis patients correlates strongly with K(2P)5.1 expression levels in CD4+ T lymphocytes in the peripheral blood
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17beta-estradiol induces the expression of KCNK5 via ERalpha(+) in breast cancer cells, and this channel plays a role in regulating proliferation in these cell lines.
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Data suggest that the cytokine receptor-coupled JAK/STAT pathway is upstream of the swelling-induced phosphorylation and activation of TASK-2 in Ehrlich ascites tumor cells.
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We here identify and characterize K2P5.1 as a critical player of T-cell effector function; selective targeting of K(2P)5.1 may hold therapeutic promise for multiple sclerosis and putatively other T-cell-mediated disorders.
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TASK-2 does not possess a histidine residue at homologous position. Inclusion of such a residue failed to produce expected increase in pH sensitivity; instead, a slight decrease was observed
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TASK-2 is not highly expressed in cerebellum
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KCNK5 is involved K(+)-channel in regulatory volume decrease in human spermatozoa, and channel activity is regulated beyond the extent of protein expression.
