anti-Potassium Channel, Subfamily K, Member 5 (KCNK5) Antibodies

Human Potassium Channel, Subfamily K, Member 5 (KCNK5) interaction partners

1. 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.

2. 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.

3. In human aldosterone-producing adrenocortical cancer cell lines, roxithromycin inhibited KCNJ5MUT-induced induction of CYP11B2 (encoding aldosterone synthase) expression and aldosterone production.

4. 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

5. These results therefore provide further structural and functional insights into the possible pathophysiological effects of this missense variant in TASK-2.

6. 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.

7. Potassium channel TASK2 drives human NK-cell proliferation and cytolytic function.

8. 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.

9. 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.

10. Potassium channels, in particular K2P channels, are expressed and functional in the apical membrane of airway epithelial cells

11. Disease activity in rheumatoid arthritis patients correlates strongly with K(2P)5.1 expression levels in CD4+ T lymphocytes in the peripheral blood

12. 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.

13. 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.

14. 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.

15. 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

16. TASK-2 is not highly expressed in cerebellum

17. KCNK5 is involved K(+)-channel in regulatory volume decrease in human spermatozoa, and channel activity is regulated beyond the extent of protein expression.

Mouse (Murine) Potassium Channel, Subfamily K, Member 5 (KCNK5) interaction partners

1. The apparent affinity of TASK-2 for membrane PI(4,5)P2 is low and it is conceivable that changing competition by intracellular polycationic compounds might mediate the previously reported sensitivity of TASK-2 to changes in cell volume. A decrease in PI(4,5)P2 by activation of Gq-PCRs is also probably responsible for TASK-2 inhibition.

2. KCNK5 channels are indispensable for the maintenance of hearing. KCNK5 is mainly found in outer sulcus Claudius', Boettcher's and root cells.

3. The data identify GPR4 and TASK-2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.

4. TASK-2 is upregulated under hypoxia in a HIF-1alpha-dependent manner in B cells.

5. The strong physiological impairment of KCNK5 in Ehrlich cells after long-term hypotonic stimulation is predominantly due to down-regulation of the KCNK5 protein synthesis.

6. data are compatible with the concept that TASK-2 channels are modulated by Gbetagamma subunits of heterotrimeric G protein; propose that this modulation is a novel way in which TASK-2 can be tuned to its physiological functions

7. alkaline-activated TASK-2 channels contribute to pH sensitivity in retrotrapezoid nucleus neurons

8. Kv1.3/TASK2 channels appear to be mainly responsible for regulatory volume decrease in murine T-lymphocytes.

9. a cycle of protonation/deprotonation of pH(o)-sensing arginine 224 side chain gates the TASK-2 channel by electrostatically tuning the conformational stability of its selectivity filter.

10. The authors report for the first time the expression of TASK-2 in B cells and surmise that the upregulation of TASK-2 by B cell receptor ligation is associated with the apoptosis of immature B cells.

11. intracellular pH, together with pH(o), is a critical determinant of TASK-2 activity and therefore of its physiological function

12. results do not support the notion that KCNK5 potassium channel mediates the capacity of inhaled anesthetics to produce immobility

13. The TASK2 channel is expressed in kidney proximal cells and could be the swelling-activated K+ channel responsible for the cell volume regulation process during osmolyte absorptions in the proximal tubules.

14. consequences of the task2 gene inactivation in mice are reminiscent of the clinical manifestations seen in human proximal renal tubular acidosis syndrome

15. Sensitivity to intracellular Na(+) may be an additional potential regulatory mechanism of TASK-2 channels.

16. pH sensing in TASK2 channels is conferred by the combined action of several charged residues in the large extracellular M1-P1 loop.

17. Cl(-) influx will be the driving force for HCO(3)(-) exit through the activation of the Cl(-)/HCO(3)(-) exchanger. This efflux of HCO(3)(-) then alkalinizes pH(e), which in turn activates TASK2 channels

18. the role of the TASK2 channel in the regulation of AVD and apoptosis phenomenon.