Small conductance calcium-activated potassium channel protein 2, also known as SK channel subtype 2 or KCNN2, KCa2.2, is a protein which in humans is encoded by the KCNN2 gene. KCNN2 is predicted to contain seven transmembrane domains with the sixth (H5) being the pore-forming domain. KCNN2 has one calmodulin binding domain. Two transcript variants encoding different isoforms have been found for the KCNN2 gene.
|Basic Information of KCNN2|
|Protein Name||Small conductance calcium-activated potassium channel protein 2|
|Aliases||KCa2.2, SK2, SKCa 2, SKCa2|
|Organism||Homo sapiens (Human)|
KCNN2 is localized in the plasma membrane depending on its interacting protein, ACTN2, a major F-actin crosslinking protein. KCNN2 is a member of the calcium-activated potassium channel family which induces membrane hyperpolarization. KCNN2 is also an integral membrane protein and always forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. KCNN2 is reported to be upregulated in failing human hearts and plays important functional roles in cardiac repolarization in atrial myocytes. KCNN2 is activated before membrane hyperpolarization and in further regulates neuronal excitability via the slow component of synaptic afterhyperpolarization (AHP). KCNN2 channels are necessary for the long-term survival of olivocochlear fibers and synapses.
This article suggests that the frissonnant (fri) mutation plays a new, potentially important physiological role, which has not been described, for the SK2 subunit of small-conductance Ca(2+)-activated potassium channels.
This article suggests that the KCNN2 gene plays an important role in the development of coronary artery aneurysms in KD.
The expression plasmid pIRES-hrGFP-SK2 is constructed successfully. The author suggests that overlapping PCR is a good choice for amplifying these genes with long size or low expression.
This article suggests that KCNN2 is closely related to VTa. It also seems that KCNN2 variants may be additional markers for risk stratification in patients susceptible to SCD.
In this article, they suggest that SK2 does not contribute to the patient's symptoms. ZNF135 is expressed in the human brain and it is likely that the homozygous mutation underlies the human phenotype.
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