Introduction of KCNA5
KCNA5, encoded by KCNA5 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, KCNA5, and other KCNA members. KCNA5 protein has 613 amino acids and contains 6 transmembrane segments (S1-S6) with a shaker-type repeat in S4. It is widely present throughout the body including the skeletal and smooth muscle, kidneys, and brain.
|Basic Information of KCNA5|
|Protein Name||Potassium voltage-gated channel subfamily A member 5|
|Aliases||HK2, HCK1, PCN1, ATFB7, HPCN1, KV1.5|
|Organism||Homo sapiens (Human)|
Function of KCNA5 Membrane Protein
KCNA5 functions as a voltage-gated potassium channel involved in the regulation of potassium ion permeability of excitable membranes. It belongs to the delayed rectifier class and regulates the recovery of resting membrane potential after depolarization. KCNA5 has been revealed to participate in the regulation of many biological processes. In the central nervous system, KCNA5 regulates the ultrarapid potassium current and involves the proliferation of microglial cells and the production and release of nitric oxide. In the heart, KCNA5 is associated with the regulation of atrial mechanical dynamics via the mediation of action potential duration of atrial myocytes. And the gain-of-function mutations or loss-of-function mutations in KCNA5 have different functional effects on atrial mechanical contraction. The gain-of-function mutations reduce the action potential duration of atrial myocytes, stabilize and enhance re-entrant excitation in atrial tissue. While the loss-of-function mutations have heterogeneous effects on action potential duration and facilitate early-after-depolarisations following beta-adrenergic stimulation. KCNA5 nonsense mutations have been shown to extend the action potential duration and involve the development of familial atrial fibrillation, even sudden cardiac death. Furthermore, KCNA5 also plays a role in pulmonary vascular function through regulating the resting membrane potential and involves pulmonary vasoconstriction during hypoxic state. In addition, KCNA5 has been reported to exert a role in the progression of tumors such as Ewing sarcoma, osteosarcoma.
Fig.1 Overview of the epigenetic repression of KCNA5 in Ewing sarcoma cancer cells. (Ryland, 2016)
Application of KCNA5 Membrane Protein in Literature
The study shows that the decreased expression of Cx40 and KCNA5 is observed in the atrial myocytes of patients with atrial fibrillation (AF). And the Cx40 mRNA levels are positively associated with the KCNA5 mRNA.
The study shows that the gain-of-function mutations or loss-of-function mutations in KCNA5 have different functional effects on atrial mechanical contraction via either decreasing or enhancing atrial output.
The study indicates that the gain-of-function mutations in KCNA5 reduce the action potential duration in single cells, and stabilize and enhance re-entrant excitation in atrial tissue. While the loss-of-function mutations in KCNA5 have heterogeneous effects on action potential duration and facilitate early-after-depolarisations following beta-adrenergic stimulation.
The study indicates that ethanol intake extends the action potential duration of atrial myocytes by suppression of ultra-rapid delayed rectified potassium currents (IKv1.5) and rapid delayed rectifier potassium currents (IhERG), which is responsible for the development of atrial fibrillation.
The study supports that KV1 play a very important role in regulating baseline coronary vascular tone, and vasodilation in response to increased transient ischemia and metabolism.
KCNA5 Preparation Options
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