Introduction of KCNT2
KCNT2, potassium channel subfamily T member 2 is a protein that in humans is encoded by the KCNT2 gene. It is also called KNa. It is also known as the Slick channel (sequence like an intermediate calcium channel), which is an outwardly rectifying potassium channel activated by internal raises in sodium or chloride ions. Channel activity of KCNT2 is inhibited by ATP and by inhalation anesthetics, such as isoflurane. It’s also inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1.
|Basic Information of KCNT2|
|Protein Name||Potassium channel subfamily T member 2|
|Aliases||Sequence like an intermediate conductance potassium channel subunit, Sodium and chloride-activated ATP-sensitive potassium channel Slo2.1, SLICK|
|Organism||Homo sapiens (Human)|
Function of KCNT2 Membrane Protein
KCNT2 is an outwardly rectifying potassium channel, which is also known as KNa or Slick channel (sequence like an intermediate calcium channel). It’s broadly expressed in ovary, lung and 22 other tissues. This channel can produce rapidly activating outward rectifier K+ currents. The channel activity can be activated by high intracellular sodium and chloride levels. Channel activity can be inhibited by ATP and by inhalation anesthetics, such as isoflurane, or upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1. The mutations in KCNT2 have been shown to be associated with the developmental and epileptic encephalopathy. In addition, mutations in KCNT2 are related with pediatric B-cell precursor acute lymphoblastic leukemia. Furthermore, KCNT2 is identified as an ATP-dependent channel which may ensure Slick’s ability and adjust electrical activity appropriately.
Fig.1 Wildtype and mutated KCNT2 and corresponding functions (Gururaj, 2017)
Application of KCNT2 Membrane Protein in Literature
This article suggests that the new spectrum of KCNT2-related disorders do not only share similar phenotypic and in vitro functional and pharmacological features with KCNT1-related disorders but also represents a further example of possible precision medicine approaches.
This article identifies non-synonymous somatic single nucleotide variants (SNVs) in KCNT2 via high-throughput sequencing in pediatric B-cell precursor acute lymphoblastic leukemia (BCP ALL).
This study indicates the mechanism of unusual altered selectivity in KCNT2 channel. It establishes pathogenicity of the Phe240Leu KCNT2 mutation in the reported EOEE patient.
This article reveals that the activity of both Slo2 channels is controlled by neuromodulators through Galphaq-protein-coupled receptors (GqPCRs). The control of Slo2.1/2.2 by neurotransmitters may cause long-lasting increases or decreases in neuronal excitability. The widespread distribution of both channels may provide a mechanism to activate or repress electrical activity in many systems of the brain.
This article identifies KCNT2 as an ATP-dependent channel, and this kind of characteristics may ensure Slick with the ability to integrate multiple indicators of the metabolic state of a cell and to adjust electrical activity appropriately.
KCNT2 Preparation Options
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