KCNK9 Membrane Protein Introduction

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
Gene Name KCNK9
Aliases TASK3, TASK-3, K2P9.1
Organism Homo sapiens (Human)
UniProt ID Q9NPC2
Transmembrane Times 4
Length (aa) 374

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.

KCNK9 Membrane Protein Introduction

Application of KCNK9 Membrane Protein in Literature

  1. Zúñiga R., et al. TASK-3 Downregulation Triggers Cellular Senescence and Growth Inhibition in Breast Cancer Cell Lines. International journal of molecular sciences. 2018, 19(4): 1033. PubMed ID: 29596383

    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.

  2. Rinné S., et al. Stress-Kinase Regulation of TASK-1 and TASK-3. Cellular Physiology and Biochemistry. 2017, 44(3): 1024-1037. PubMed ID: 29179200

    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.

  3. Bohnen M.S., et al. The Impact of Heterozygous KCNK3 Mutations Associated With Pulmonary Arterial Hypertension on Channel Function and Pharmacological Recovery. Journal of the American Heart Association. 2017, 6(9): e006465. PubMed ID: 28889099

    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.

  4. Wright P.D., et al. Terbinafine is a novel and selective activator of the two-pore domain potassium channel TASK3. Biochemical and biophysical research communications. 2017, 493(1): 444-450. PubMed ID: 28882594

    The authors firstly identified Terbinafine as a novel and selective activator of two-pore domain potassium channel TASK3.

  5. Grandone A., et al. Molecular Screening of MKRN3, DLK1, and KCNK9 Genes in Girls with Idiopathic Central Precocious Puberty. Hormone research in paediatrics. 2017, 88(3-4): 194-200. PubMed ID: 28672280

    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

To obtain the soluble and functional target protein, Creative Biolabs has developed the versatile Magic™ membrane protein production platform to provide many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-KCNK9 antibody development services.

In recent years, Creative Biolabs has successfully generated many functional membrane proteins for our customers. We are happy to tailor one-stop, custom-oriented service packages regarding a variety of membrane protein targets. Please feel free to contact us for more information.

All listed customized services & products are for research use only, not intended for pharmaceutical, diagnostic, therapeutic or any in vivo human use.

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