mProX™ Human KCNK3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 DDSA mutations produce a gain-of-function phenotype in TASK-1.
Typical TEVC recordings of WT TASK-1 and DDSA mutant currents in response to 20 mV voltage steps from a holding potential of -80 mV to +50 mV.
Ref: Sörmann, Janina, et al. "Gain-of-function mutations in KCNK3 cause a developmental disorder with sleep apnea." Nature Genetics 54.10 (2022): 1534-1543.
Pubmed: 36195757
DOI: 10.1038/s41588-022-01185-x
Research Highlights
The two-pore domain potassium channel family includes TWIK-related acid-sensitive potassium channel 1 (TASK-1 encoded by KCNK3). This gene subfamily has been specifically connected to the human pulmonary circulation and is constitutively active in excitable cells, such as smooth muscle cells, at physiological resting membrane potentials.
Olschewski, Andrea, et al. "TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications." European Respiratory Journal 50.5 (2017).
Pubmed:
29122916
DOI:
10.1183/13993003.00754-2017
KCNK3 expression and activity in pulmonary artery smooth muscle cells and endothelial cells are markedly decreased in PAH and experimental PH. Increased proliferation, vasoconstriction, and inflammation were all encouraged by KCNK3 inhibition. Monocrotaline-induced PH was lessened when KCNK3 was pharmacologically activated in vivo, indicating that KCNK3 depletion is a critical step in the genesis of PAH and may therefore be addressed therapeutically.
Antigny, Fabrice, et al. "Potassium channel subfamily K member 3 (KCNK3) contributes to the development of pulmonary arterial hypertension." Circulation 133.14 (2016): 1371-1385.
Pubmed:
26912814
DOI:
10.1161/CIRCULATIONAHA.115.020951