Small conductance calcium-activated potassium channel 3 (KCNN3), also known as KCa2.3, is a protein that in humans is encoded by the KCNN3 gene, which is mapped to the chromosome 1q21.3. It is a member of small-conductance potassium channel family, which consists of three members - KCNN1, KCNN2, and KCNN3 sharing 60-70% sequence identity. KCNN3 contains an intracellular N and C termini and six highly conserved transmembrane segments. There are two arrays of polyglutamine (CAG trinucleotide) repeats in the N terminal region.
|Basic Information of KCNN3|
|Protein Name||Small conductance calcium-activated potassium channel protein 3|
|Aliases||KCa2.3, SK3, SKCa 3, SKCa3|
|Organism||Homo sapiens (Human)|
KCNN3 forms a voltage-independent potassium channel activated by intracellular calcium and is involved in a wide array of physiological processes. KCNN3 is reported to contribute to the development and progression of numerous solid tumors. In melanoma cells, upregulation of KCNN3 enhances cell motility pathways by hyperpolarizing the cell membrane potential. KCNN3 is a mediator of cell migration and cysteine cathepsin-dependent cell invasiveness in breast cancer cells. The expression level of KCNN3 channels in the endothelium influences arterial tone via arterial smooth muscle membrane potential. Mutations in KCNN3 are always related to serious neurological disorders, including schizophrenia, bipolar disorder, Alzheimer's disease, anorexia nervosa, and ataxia as well as myotonic muscular dystrophy.
Fig.1 Schematic model of the proposed endocytosis and recycling of KCa2.3 at the plasma membrane. (Bertuccio, 2018)
The article identifies common genetic variants underlying lone AF. The authors identify an association on chromosome 1q21 to lone AF and replicate this association in two independent cohorts with lone AF rs13376333 is intronic to KCNN3, which encodes a potassium channel protein involved in atrial.
The results are opposed to the view that larger KCNN3 alleles are preferentially related with schizophrenia in individuals from multiply affected families.
Their data do not support the involvement of the KCNN3 (hSKCa3) gene in the etiology of schizophrenia as no intergenerational CAG repeat instability was detected.
This article suggests that KCNN3 genotypes modify cognitive performance, shown here in a large sample of schizophrenic patients. Reduction of SK3 function may constitute a pharmacological target to improve cognition in schizophrenia and other conditions with cognitive impairment.
The authors show a relationship between OIN and CAG repeat polymorphisms of the KCNN3 gene in a preclinical model.
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