KCNE2 Membrane Protein Introduction

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
Gene Name KCNE2
Aliases MinK-related peptide 1, Minimum potassium ion channel-related peptide 1, Potassium channel subunit beta MiRP1
Organism Homo sapiens (Human)
UniProt ID Q9Y6J6
Transmembrane Times 1
Length (aa) 123

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.

KCNE2 Membrane Protein Introduction Fig.1 KCNE2 is a β-subunit for multiple cardiac ion currents. (Roberts, 2017)

Application of KCNE2 Membrane Protein in Literature

  1. Iivonen A.P., et al. Screening for germline KCNQ1 and KCNE2 mutations in a set of somatotropinoma patients. Endocr Connect. 2018, 7(5): 645-652. PubMed ID: 29703730

    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.

  2. Roberts J.D., et al. Loss-of-function KCNE2 variants: True monogenic culprits of long-QT syndrome or proarrhythmic variants requiring secondary provocation? Circ Arrhythm Electrophysiol. 2017, 10(8). PubMed ID: 28794082

    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.

  3. Lee S.M., et al. Kcne2 deletion impairs insulin secretion and causes type 2 diabetes mellitus. FASEB J. 2017, 31(6): 2674-2268. PubMed ID: 28280005

    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.

  4. Hu Z., et al. Kcne2 deletion attenuates acute post-ischaemia/reperfusion myocardial infarction. Cardiovasc Res. 2016, 110(2): 227-237. PubMed ID: 26952045

    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.

  5. Neethling A., et al. Filamin C: a novel component of the KCNE2 interactome during hypoxia. Cardiovasc J Afr. 2016, 27(1): 4-11. PubMed ID: 26956495

    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

To gain soluble and functional protein targets, we have established systematic reconstitution forms and active formats for these membrane proteins. Our robust Magic™ membrane protein production platform presents numerous options for customers to flexibly choosing to achieve their purposes. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-KCNE2 antibody development services.

Creative Biolabs as a forward-looking institute has won great recognition among researchers for successfully completed projects. Here, we are proud to introduce our one-step, customized membrane protein preparation services in required formats for worldwide clients. Please feel free to contact us for more details.


  1. Roberts J D, et al. (2017). Loss-of-function KCNE2 variants: true monogenic culprits of long-qt syndrome or proarrhythmic variants requiring secondary provocation? Circ Arrhythm Electrophysiol. 10(8).

Online Inquiry

Verification code
Click image to refresh the verification code.


USA: 45-1 Ramsey Road, Shirley, NY 11967, USA
Europe: Heidenkampsweg 58, 20097 Hamburg, Germany
Call us at:
USA: 1-631-381-2994
Europe: 44-207-097-1828
Fax: 1-631-207-8356
Our customer service representatives are available 24 hours a day, 7 days a week. Contact Us