KCNA6 Membrane Protein Introduction

Introduction of KCNA6

KCNA6, encoded by KCNA6 gene, is a member of potassium channel, voltage-gated, shaker-related subfamily which regulates the transportation of potassium ions across the membrane in accordance with their electrochemical gradient. The functional potassium channels are homotetrameric or heterotetrameric. And heterotetrameric channels contain four members such as KCNA1, KCNA2, KCNA4, KCNA6 as well as other KCNA members. KCNA6 protein has 529 amino acids and contains 6 transmembrane segments (S1-S6) with a shaker-type repeat in S4.

Function of KCNA6 Membrane Protein

KCNA6 belongs to the voltage-gated potassium channel family which mediates potassium ion permeability of excitable membranes. It is involved in the regulation of neurotransmitter release, heart rate, neuronal excitability, insulin secretion, smooth muscle contraction, epithelial electrolyte transport, and cell volume. Kv1 channels have been revealed to mediate dendrotoxin-sensitive K⁺ currents. The heteromeric Kv1 channels with a single Kv1.1, Kv1.2, or Kv1.6 protein are widely present in the nervous system where they confer dendrotoxin sensitivity. Moreover, Kv1 channels in the brain are involved in the neurologic manifestations and neoplasms. It has been shown the members of the Shaker-related voltage-gated potassium channel family such as KCNA1, KCNA2, and KCNA6 are associated with metastatic neoplasms and paraneoplastic syndromes including infections from herpes simplex and zoster, or other viral agents, Wernicke's encephalopathy, Leigh's disease, leptomeningeal carcinomatosis, and cancer-unrelated encephalitis. Evaluation for voltage-gated potassium channel antibodies has been indicated as the effective autoimmune serologic assay of subacute idiopathic nervous system disorders.

Fig.1 K⁺ channel structural topology. (Naranjo, 2016)

Application of KCNA6 Membrane Protein in Literature

1. Silver K., et al. Inhibition of Kv channel expression by NSAIDs depolarizes membrane potential and inhibits cell migration by disrupting calpain signaling. Biochemical Pharmacology. 2015, 98(4):614-628. PubMed ID: 26549367
   
   

   The study reveals that the inhibition of epithelial cell migration by non-steroidal anti-inflammatory drugs (NSAIDs) is related to the reduction of Kv channel subunit expression, and provides a mechanism for NSAIDs to inhibit cell migration, possibly leading to NSAIDs induced gastrointestinal (GI) toxicity.

2. Raimondi L., et al. Methylamine-dependent release of nitric oxide and dopamine in the CNS modulates food intake in fasting rats. British Journal of Pharmacology. 2007, 150(8):1003-1010. PubMed ID: 17339841
   
   

   The study indicates that the release of nitric oxide and dopamine in the hypothalamus mediated by methylamine regulates food intake in fasting rats, which is the result of Kv1.6 channel interactions.

3. Saito M., et al. Two opposing roles of 4-AP-sensitive K⁺ current in initiation and invasion of spikes in rat mesencephalic trigeminal neurons. J Neurophysiol. 2006, 96(4):1887-901. PubMed ID: 16624997
   
   

   The study shows that the strong immune activity of Kv1.1 and Kv1.6 is detected in the soma but not in the stem axon of mesencephalic trigeminal nucleus neurons.

4. Iwasaki S., et al. Developmental changes in the expression of Κv1 potassium channels in rat vestibular ganglion cells. Brain Research. 2012, 1429:29-35. PubMed ID: 22079321
   
   

   The study suggests that the decreased Kv1.6 protein and mRNA may be related to the maturation of primary vestibular excitability.

5. Tan K.M., et al. Clinical spectrum of voltage-gated potassium channel autoimmunity. Neurology. 2008, 70(20):1883-90. PubMed ID: 18474843
   
   

   The study expands the insight of spectrum of neurologic manifestations and neoplasms related to voltage-gated potassium channel (VGKC) autoimmunity.

KCNA6 Preparation Options

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Reference

1. Naranjo D, et al. (2016). Pore size matters for potassium channel conductance. Journal of General Physiology. 148(4): 277-91.

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