Introduction of KCNE2
KCNE2, also known as potassium voltage-gated channel subfamily E regulatory subunit 2, potassium channel, voltage gated subfamily E regulatory beta subunit 2, potassium voltage-gated channel, Isk-related family, member 2, cardiac voltage-gated potassium channel accessory subunit 2, voltage-gated K+ channel subunit MIRP1, potassium channel subunit, MiRP1, ATFB4, MIRP1, LQT5, or LQT6, is a membrane protein of about 14.5 k Da that is composed of 123 amino acids. In humans, it is encoded by the KCNE2 gene located at chromosome 21q22.11. The KCNE2 gene codes for a MiRP1 protein, which is now more commonly referred to KCNE2. It can assemble with many alpha subunits of voltage-gated cation channels and regulate their gating, and conductance. KCNE2 is expressed in heart and stomach, as well as in lung, kidney, bladder, brain, skeletal muscle, and spinal cord.
|Basic Information of KCNE2|
|Protein Name||Potassium voltage-gated channel subfamily E member 2|
|Aliases||MinK-related peptide 1, Minimum potassium ion channel-related peptide 1, Potassium channel subunit beta MiRP1|
|Organism||Homo sapiens (Human)|
Function of KCNE2 Membrane Protein
KCNE2 is a member of a family with small auxiliary subunits of voltage-gated cation channels and has been reported to play a key role in maintaining cardiac electrical stability. It modulates hERG potassium channels and KCNE2-hERG complexes are thought, in part, to generate the cardiac IKr current, a major repolarizing force in human ventricles. Mutations in the KCNE2 gene are correlated with a type of inherited long QT syndrome, LQT6. In addition to its interaction with hERG, it is also found to modulate other voltage-gated potassium α subunits in heterologous co-expression research, such as KCNQ1 (Kv7.1), Kv3.1, Kv3.2, and Kv4.2. Impacts of KCNE2 on KCNQ1 are extremely dramatic. It converts KCNQ1 to a voltage-independent “leak” channel that keeps K+ selectivity but is constitutively active regardless of membrane potential. Aside from its role in human heart, KCNQ1 is necessary for the normal gastric acid secretion and is supposed to provide a K+ ion efflux in parietal cells of gastric glands to balance K+ ion influx by the gastric H+/K+-ATPase.
Fig.1 KCNE2 is a β-subunit for multiple cardiac ion currents. (Roberts, 2017)
Application of KCNE2 Membrane Protein in Literature
KCNQ1 and KCNE2 were screened for germline mutations in 53 acromegaly patients by Sanger sequencing. And impacts of variants were predicted by in silico tools. Although larger patient series were needed to confirm these findings, either KCNQ1 or KCNE2 mutations did not seem to explain the formation of somatotropinoma.
On the basis of clinical phenotype and certain database, the findings suggested that numerous KCNE2 variants, and perhaps all, had been erroneously recognized as LQTS-causative mutations. Conversely, KCNE2 variants probably confer proarrhythmic susceptibility when induced by additional environmental or genetic factors, or both.
The results in this article demonstrated that KCNE2 was necessary for normal β-cell electrical activity and insulin secretion, and the deletion of Kcne2 resulted in T2DM. KCNE2 was likely to regulate multiple K+ channels in β cells, such as the T2DM-linked KCNQ1 potassium channel α subunit.
Kcne2 deletion preconditioned the heart, moderating the acute tissue damage induced by an imposed ischaemia/reperfusion injury (IRI). The findings provided further proof that genetic disruption of arrhythmia-related ion channel genes had cardiac ramifications beyond abnormal electrical activity.
The identification of filamin C (FLNC) as a novel KCNE2 ligand not only enhanced current understanding of ion channel regulation and function, but also contributed valuable information of possible pathways likely to be implicated in long-QT syndrome (LQTS) pathogenesis.
KCNE2 Preparation Options
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