KCNE2

Official Full Name

potassium voltage-gated channel subfamily E regulatory subunit 2

Organism

Homo sapiens

GeneID

9992

Background

Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage-gated, isk-related subfamily. This member is a small integral membrane subunit that assembles with the KCNH2 gene product, a pore-forming protein, to alter its function. This gene is expressed in heart and muscle and the gene mutations are associated with cardiac arrhythmia. [provided by RefSeq, Jul 2008]

Synonyms

LQT5; LQT6; ATFB4; MIRP1;

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Detailed Information

Recent Research

KCNE2, also called MinK-related peptide MiRP1, is a member of the small auxiliary subunits of voltage-gated cation channels encoded by KCNE family gene, members of which each encode a single-pass membrane protein. KCNE2 is expressed in human heart but is also particularly enriched in certain secretory epithelia, including gastric parietal cells. KCNE2 modulates cardiac Kv alpha subunits human eag-related gene (HERG) and KCNQ1 in vitro. In parietal cells, KCNE2 forms complexes with the KCNQ1 voltage-gated potassium channel pore-forming (α) subunit, resulting in a remarkable transformation. KCNE proteins can regulate most aspects of Kv channel biology, from channel biogenesis itself through to gating, selectivity and conductivity of functional channels at the membrane, and even channel internalization from the membrane.

It has been found that KCNE2 deletion impairs hyperpolarization-activated, cyclic nucleotide-gated (HCN) channel function in cortical-thalamic relay neurons, suggesting the possibility of HCN-KCNE2 complexes in mammalian brain. In addition, KCNE2 can also reportedly regulate the cardiac voltage-gated calcium channel, Cav_1.2, forming complexes with reduced activity compared to channels lacking KCNE2, possibly mediated through the Cav_1.2 N-terminal inhibitory module. KCNE2 can also regulate Kv channels that are expressed in the brain. It has been shown that, KCNE2 deletion in mice causes a multisystem syndrome that adversely impacts the heart, generating both electrical disturbances and creating an ischaemic substrate.

Furthermore, KCNE2 is important in maintaining the cardiac electrical stability because mutations or a polymorphism in KCNE2 have been linked to long QT syndrome (LQT6) and familial atrial ﬁbrillation/short QT syndrome. Targeted deletion of KCNE2 impairs ventricular repolarization and predisposes the heart to arrhythmia. Among the KCNE subunits, KCNE2 has the most promiscuity of function which can coassemble with multiple α-subunits of voltage-dependent cation channels and modulate their gating, conductance and pharmacology. Heretofore, heterologously expressed KCNE2 has been demonstrated to regulate hERG, KCNQ1–3, Kv3.1, Kv3.2, Kv4.2, Kv4.3, Kv1.5, and HCN (pacemaker) cardiac ion channel α subunits.

References:

Abbott G W. The KCNE2 K+ channel regulatory subunit: ubiquitous influence, complex pathobiology. Gene, 2015, 569(2):162-172.
Tinel N, et al. KCNE2 confers background current characteristics to the cardiac KCNQ1 potassium channel. Embo Journal, 2014, 19(23):6326-6330.
W Liu, J Deng, et al. KCNE2 modulates cardiac L-type Ca(2+) channel. Journal of Molecular and Cellular Cardiology, 2014, 72(7):208-218.
Lee S M, et al. Kcne2 deletion promotes atherosclerosis and diet-dependent sudden death. Journal of Molecular & Cellular Cardiology, 2015, 87:148-151.

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