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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints.
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On the basis of clinical phenotype, the high allelic frequencies of LQT6 mutations in the Exome Aggregation Consortium database, and absence of previous documentation of genotype-phenotype segregation, our findings suggest that many KCNE2 variants, and perhaps all, have been erroneously designated as LQTS-causative mutations. Instead, KCNE2 variants may confer proarrhythmic susceptibility when provoked by additional envir
These results demonstrate that KCNE2 is required for normal beta-cell electrical activity and insulin (show INS Proteins) secretion, and that Kcne2 deletion causes T2DM.
The identification of Filamin C (show FLNC Proteins) as a novel KCNE2 ligand not only enhances current understanding of ion channel function and regulation, but also provides valuable information about possible pathways likely to be involved in long-QT syndrome pathogenesis
KCNE2 has been widely studied since its role in the heart was discovered; it is association with inherited and acquired human Long QT syndrome; physiological analyses together with genetics studies have uncovered a startling array of functions for KCNE2, in the heart, stomach, thyroid and choroid plexus. [Review]
Women with elevated BMI have enhanced hERG (show KCNH2 Proteins) activity as a result of low beta-inhibitory protein expression, which likely contributes to weak contractions and poor labour outcomes.
M54T MiRP1 mutation axecerbate drug-induced long QT syndrome and arrhythmia.
The effect of KCNE2 mutations on KV7.1 (show KCNQ1 Proteins) was abolished in the presence of the major IKs beta-subunit (show POLG Proteins) KCNE1 (show KCNE1 Proteins), when coexpressed in a 1:1:1 molar ratio.
Mutations in KCNE2 has been shown to cause familial atrial fibrillation.
The transmembrane domains (TMDs) of KCNE1 (show KCNE1 Proteins) and KCNE2 were illustrated to associate with the KCNQ1 (show KCNQ1 Proteins) channel in different modes.
study concluded that the variants in KCNQ1 (show KCNQ1 Proteins), KCNH2 (show KCNH2 Proteins), KCNE1 (show KCNE1 Proteins) and KCNE2 genes may be correlated with the occurrence of part of sudden unexplained nocturnal death syndrome cases in southern China
Kcne2 deletion preconditions the heart, attenuating the acute tissue damage caused by an imposed ischaemia/reperfusion injury
The data establish causality for the first example of ion channel-linked atherosclerosis, and demonstrate that the severity of Kcne2-linked cardiac arrhythmias is strongly diet-dependent.
Endogenous KCNE2 in cardiomyocytes is important in maintaining cardiac electrical stability mainly by regulating Ito and action potential duration.
Kcne2-deficient mice, in addition to the previously reported phenotypes, also present with iron-deficient anemia.
KCNQ1 (show KCNQ1 Proteins), KCNE2, and SMIT1 (show SLC5A3 Proteins) form reciprocally regulating complexes that affect neuronal excitability.
The Kcne2 Deletion suggest that a more holistic view of the pathogenesis of monogenic cardiac arrhythmias could provide a clearer picture of the mechanisms underlying sudden cardiac dealth.
KCNE1 (show KCNE1 Proteins) and KCNE2, auxiliary subunits of voltage-gated potassium channels, undergo sequential cleavage mediated by either alpha-secretase and presenilin(PS)/gamma-secretase or BACE1 (show BACE Proteins) and PS/gamma-secretase in cells.
Loss of KCNE2 leads to downregulation of HCN channel function associated with increased excitability in neurons in the cortico-thalamo-cortical loop.
KCNE2 influences blood-CSF (show CSF2 Proteins) anion flux by regulating KCNQ1 (show KCNQ1 Proteins) and KCNA3 (show KCNA3 Proteins) in the choroid plexus epithelium.
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.
cardiac voltage-gated potassium channel accessory subunit 2
, minK-related peptide 1
, minK-related peptide-1
, minimum potassium ion channel-related peptide 1
, potassium channel subunit beta MiRP1
, potassium channel subunit, MiRP1
, potassium voltage-gated channel subfamily E member 2
, voltage-gated K+ channel subunit MIRP1
, potassium voltage-gated channel, Isk-related subfamily, gene 2
, MinK-related peptide 1
, potassium channel beta subunit
, K+/pacemaker channel beta subunit mirp1
, minimum potassium ion channel related peptide 1