Introduction of KCNK9
Potassium channel subfamily K member 9 (KCNK9), also known as TASK3, TASK-3, K2P9.1, is encoded by gene KCNK9. KCNK9 is classified into the superfamily of potassium channel proteins containing two pore-forming P domains (K2P). KCNK9 is widely expressed in neurons of the central nervous system, including the cerebellar granule cells, locus coeruleus, motor neurons, pontine nuclei, some cells in the neocortex, habenula, olfactory bulb granule cells, and cells in the external plexiform layer of the olfactory bulb, where it contributes to generating resting and action potentials. In addition, KCNK9 is also expressed in the hippocampus; both on pyramidal cells and interneurons.
|Basic Information of KCNK9|
|Protein Name||Potassium channel subfamily K member 9|
|Aliases||TASK3, TASK-3, K2P9.1|
|Organism||Homo sapiens (Human)|
Function of KCNK12 Membrane Protein
Except for the contribution for the resting and action potentials in CNS, KCNK9 has been recognized for its potential oncogenic properties. It has been reported that KCNK9 is significantly overexpressed in human breast and lung tumors, in ovarian tumors, in colorectal cancer and melanoma, etc. Heterologous overexpression of KCNK9 has been shown to induce tumorigenesis in experimental animal models, confirming its oncogenic properties. It has been documented that gain of function of KCNK9 is associated with the acquisition of several malignant characteristics, including resistance to hypoxia and serum deprivation. Monoclonal antibodies against the cap domain of KCNK9 can inhibit tumor growth and metastasis in animal models with no significant side effects, suggesting its great therapeutic potential.
Application of KCNK9 Membrane Protein in Literature
In this article, the authors used small hairpin RNA (shRNA)-mediated knockdown to identify the effect of reducing the expression of TASK-3 in MDA-MB-231 and MCF-10F human mammary epithelial cell lines and they found that knocking down TASK-3 would reduce cell proliferation, implicating TASK-3 as a critical factor in cell cycle progression.
This article revealed that serum- and glucocorticoid-inducible kinases (SGKs) and proteinkinase B (PKB) induced a strong, dose- and time-dependent current reduction of TASK-1 and TASK-3. And SGK co-expression reduced the surface expression of TASK-1/3, leading to a predominant localization of the channels into late endosomes.
This article demonstrated that heterozygous KCNK3 mutations in PAH led to the variable loss of channel function via distinct mechanisms and homomeric or heterodimeric mutant KCNK3 channels represented novel therapeutic substrates in PAH.
The authors firstly identified Terbinafine as a novel and selective activator of two-pore domain potassium channel TASK3.
The authors sequenced MKRN3, DLK1, and KCNK9 coding regions in 60 girls with idiopathic CPP (familial in 23 cases) and they revealed that point mutations in DLK1 and KCNK9 at least did not seem to be a common cause of CPP in girls.
KCNK9 Preparation Options
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