mProX™ Human KCNN3 Stable Cell Line

Product Information

Target Protein

KCNN3

Target Family

SKCa

Target Protein Species

Human

Host Cell Type

CHO-K1; HEK293

Target Classification

Ion Channel Cell Lines

Target Research Area

Cardiovascular Research; CNS Research

Related Diseases

Zimmermann-Laband Syndrome; Zimmermann-Laband Syndrome

Gene ID

3782

UniProt ID

Q9UGI6

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

Activated by intracellular calcium, KCNN3 creates a voltage-independent potassium channel and is involved in numerous physiological functions. It has been observed that KCNN3 plays a role in the initiation and advancement of several solid tumors. By hyperpolarizing the potential of the cell membrane, KCNN3 overexpression in melanoma cells improves the pathways involved in cell motility. In breast cancer cells, KCNN3 mediates both cell migration and invasiveness that is dependent on cysteine cathepsin. Via the arterial smooth muscle membrane potential, the endothelium's expression of KCNN3 channels affects arterial tone. Serious neurological conditions such as schizophrenia, bipolar disorder, Alzheimer's disease, anorexia nervosa, ataxia, and myotonic muscular dystrophy are consistently associated with mutations in KCNN3. The customized KCNN3 stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

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Published Data

Fig.1 Functional Expression of Wild-Type (WT) and Mutant KCNN3 Channels in CHO Cells

Reveals variations in the channel activation process CHO cells heterologously expressing wild-type (WT), p.Lys269Glu (K269E), p.Gly350Asp (G350D), p.Ser436Cys (S436C), or p.Val450Leu (V450L) KCNN3 channels were used to make whole-cell recordings. Cells were cultured in Ringer solution with a strongly reduced (nominal 50 nM) Ca2+ concentration for at least 10 minutes before the recordings in order to achieve intracellular low Ca2+ levels. The nominal free Ca2+ content in the pipette solution was 1 mM.

Ref: Bauer, Christiane K., et al. "Gain-of-function mutations in KCNN3 encoding the small-conductance Ca2+-activated K+ channel SK3 cause Zimmermann-Laband syndrome." The American Journal of Human Genetics 104.6 (2019): 1139-1157.

Pubmed: 31155282

DOI: 10.1016/j.ajhg.2019.04.012

Research Highlights

Using RNA-sequencing, a large number of dysregulated genes have been found. The association between LVEF and CACNG8, KCNN3 and KCNJ2 as well as the up-regulation of KCNN3 and KCNJ2 in all SMVT patients, regardless of CACNG8 expression, point to a major involvement of these three-ion flux related genes in the LV dysfunction seen in this cardiomyopathy. Additionally, there is a significant correlation between the presence of SMVT and the up-regulation of KCNN3 and KCNJ2.
Ortega, Ana, et al. "Patients with dilated cardiomyopathy and sustained monomorphic ventricular tachycardia show up-regulation of KCNN3 and KCNJ2 genes and CACNG8-linked left ventricular dysfunction." PloS one 10.12 (2015): e0145518.
Pubmed: 26710323 DOI: 10.1371/journal.pone.0145518

To look into the connection between the single-nucleotide polymorphism (SNP) rs13376333 in KCNN3 and the risk of atrial fibrillation (AF) and to offer suggestions for AF therapy and prevention.
Yao, Jia-Lu, et al. "KCNN3 SNP rs13376333 on chromosome 1q21 confers increased risk of atrial fibrillation." International Heart Journal 56.5 (2015): 511-515.
Pubmed: 26370375 DOI: 10.1536/ihj.15-133