KCNC3 Membrane Protein Introduction

Introduction of KCNC3

KCNC3, also known as Kv3.3, is an integral membrane protein that belongs to the Kv3 subfamily of voltage-gated potassium channels. The Kv3 subfamily is composed of the subunits Kv3.1-3.4 that can be constructed as either homotetrameric potassium channels or heterotetrameric potassium channels. KCNC3 protein encoded by the KCNC3 gene has 757 amino acid residues and contains 6 transmembrane segments (S1-S6) with a voltage-sensor in S4. It is primarily expressed in the brain and kidney.

Function of KCNC3 Membrane Protein

KCNC3 is a voltage-gated potassium channel that plays an important role in the transportation of potassium ions across the membrane in accordance with their electrochemical gradient. The channel can alter its opened or closed conformations in response to the voltage difference across the membrane, thereby controlling potassium ion permeability of excitable membranes. It has been revealed that KCNC3 is involved in the rapid repolarization of fast-firing brain neurons via mediating outward potassium current. The potassium channel belongs to delayed rectifier class of channel proteins displaying rapid activation and inactivation kinetics. KCNC3 has been suggested to regulate the frequency, duration, and shape of action potentials in Purkinje cells. Moreover, KCNC3 also involves in the regulation of the duration and frequency of action potentials that further regulate the activity of voltage-gated Ca²⁺ channels activity and cellular Ca²⁺ homeostasis, required in the normal survival of cerebellar neurons. In addition, mutations in human KCNC3 may be the cause of spinocerebellar ataxia. And KCNC3 knockout mice may display the impaired gait and decreased motor performance, which is related to abnormal discharge of Purkinje cells and abnormal cerebellar system.

Fig.1 KCNC3 mutations lead to amino acid substitutions in highly conserved domains. (Waters, 2006)

Application of KCNC3 Membrane Protein in Literature

1. Khare S., et al. A KCNC3 mutation causes a neurodevelopmental, non-progressive SCA13 subtype associated with dominant negative effects and aberrant EGFR trafficking. Plos One. 2017, 12(5):e0173565. PubMed ID: 28467418
   
   

   The study identifies that the KCNC3 R423H allele is a cause of a neurodevelopmental, non-progressive spinocerebellar ataxia subtype.

2. Zhang Y., et al. Kv3.3 potassium channels and spinocerebellar ataxia. Journal of Physiology. 2015, 594(16):4677-84. PubMed ID: 26442672
   
   

   The study reviews the KCNC3 localization and physiological function in the central nervous system and the association between disease-causing mutations and function of the channel.

3. Khare S., et al. C-terminal proline deletions in KCNC3, cause delayed channel inactivation and an adult-onset progressive SCA13 with spasticity. Cerebellum. 2018, 17(5):692-697. PubMed ID: 29949095
   
   

   The findings show that the intracellular C-terminal portion of Kv3.3 exerts the very important role in the ion channel function and possesses the clinical importance.

4. Duarri A., et al. Functional analysis helps to define KCNC3 mutational spectrum in Dutch ataxia cases. Plos One. 2015, 10(3):e0116599. PubMed ID: 25756792
   
   

   The study identifies at least one novel pathogenic mutation of KCNC3 gene that is a cause of spinocerebellar ataxia and two additionally potential spinocerebellar ataxia mutations.

5. Song M.S., et al. Voltage-gated K⁺ channel, Kv3.3 is involved in hemin-induced K562 differentiation. Plos One. 2015, 11(2):e0148633. PubMed ID: 26849432
   
   

   The study reveals that the voltage-gated K⁺ channels Kv3.3 may be involved in the hemin-induced K562 differentiation, which provides important information regarding vital cellular processes.

KCNC3 Preparation Options

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Reference

1. Waters M F, et al. (2006). Mutations in the voltage-gated potassium channel KCNC3 cause degenerative and developmental CNS phenotypes. Nature Genetics. 38(4): 447-51.

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