KCNT2 Membrane Protein Introduction

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 K_Na. 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.

Function of KCNT2 Membrane Protein

KCNT2 is an outwardly rectifying potassium channel, which is also known as K_Na 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

1. Ambrosino P., et al. De novo gain-of-function variants in KCNT2 as a novel cause of developmental and epileptic encephalopathy. Ann Neurol. 2018, 83(6):1198-1204. PubMed ID: 29740868
   
   

   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.

2. Gunnarsson R., et al. Mutation, methylation, and gene expression profiles in dup(1q)-positive pediatric B-cell precursor acute lymphoblastic leukemia. Leukemia. 2018, 32(10):2117-2125. PubMed ID: 29626196
   
   

   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).

3. Gururaj S., et al. A De Novo Mutation in the Sodium-Activated Potassium Channel KCNT2 Alters Ion Selectivity and Causes Epileptic Encephalopathy. Cell Rep. 2017, 21(4):926-933. PubMed ID: 29069600
   
   

   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.

4. Santi C.M., et al. Opposite regulation of Slick and Slack K⁺ channels by neuromodulators. J Neurosci. 2006, 26(19):5059-68. PubMed ID: 16687497
   
   

   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.

5. Bhattacharjee A., et al. Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP. J Neurosci. 2003, 23(37):11681-91. PubMed ID: 14684870
   
   

   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.

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Reference

1. Gururaj S, et al. (2017). A De Novo Mutation in the Sodium-Activated Potassium Channel KCNT2 Alters Ion Selectivity and Causes Epileptic Encephalopathy. Cell Rep. 21(4):926-933.

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