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We propose that KCNE1 moves the S5-P-helix loop of KV7.1 towards the polyunsaturated fatty acid-binding site, which indirectly causes polyunsaturated fatty acid protonation, thereby reducing the effect of polyunsaturated fatty acids on KV7.1.
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relatively common variants in KCNE1 may result in a mild QT phenotype designated as "LQT5-Lite" to distinguish such potentially proarrhythmic common variants (ie, functional risk alleles) from rare pathogenic variants that truly confer monogenic disease susceptibility, albeit with incomplete penetrance.
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S38G mutation induced a loss-of-function of IKs due to decreasing of KCNE1 protein expression and defecting in KCNE1 protein membrane trafficking
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All the protein systems generated through these processes were refined by long Molecular Dynamics simulations. The refined models were analyzed extensively to infer data about the interaction of KCNQ1 channel with its accessory KCNE1 beta subunits.
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In lesion samples collected from children with cardiac insufficiency, for Mink-S27, we detected significant difference in AA, CC genotype frequency and allele frequency between the observation group and the control group
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SUMOylation of KCNQ1 is KCNE1 dependent and determines the native attributes of cardiac IKs in vivo.
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Equine KV7.1/KCNE1 expressed in CHO-K1 cells exhibited electrophysiological properties that are overall similar to the human orthologs; however, a slower deactivation was found which could result in more open channels at fast rates.
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The KCNE1 (rs1805127) appears to an independent risk factor for AF in the Uygur population. And the KCNE4 (rs12621643) was an independent risk factor for AF among both Uygurs and Hans.
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Western blotting analysis combined with these pharmacological data suggest that long-term insulin treatment augments KCNQ1/KCNE1 currents by increasing KCNE1 protein expression.
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KCNQ1/KCNE1 channel does not require phosphatidylinositol-4,5-bisphosphate (PIP2) or phosphatidylinositol-4-phosphate for anterograde trafficking, but is heavily reliant on PIP2 for channel function once at the plasma membrane.
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The genetic variant rs426496 in AQP2; rs591810 in AQP3 and rs1805127, rs1805128, and rs17173510, in KCNE1 were found in patients with Meniere's disease
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Meta-analysis suggests that the G38S polymorphism in the KCNE1 gene can significantly increase the risk of atrial fibrillation in both Chinese and white individuals.
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Sphingomyelin synthase 1 positively regulates KCNQ1/KCNE1 channel density in a protein kinase D-dependent manner.
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Receptor Species-dependent Desensitization Controls KCNQ1/KCNE1 K+ Channels as Downstream Effectors of Gq Protein-coupled Receptors.(
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KCNE1 encodes a modulator of KCNQ1 and KCNH2 channels. Long QT syndrome (LQTS) patients with KCNE1(G38S) had a rate-dependent repolarization abnormality similar to patients with LQT2 and, therefore, may have a potential risk to develop lethal arrhythmias.
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A stoichiometry of 4:4 between the alpha KCNE1 and the beta KCNQ1-subunits has been established.
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Based on current evidence from published studies, neither of the two variants from KCNE was significantly associated with the risk of Meniere's disease--{REVIEW}
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Analysis of QT-RR relationship could also evaluate the latent arrhythmogenicity of KCNE1(G38S).
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The incidence of AF among the senior Uygur population in Xinjiang territory was correlated with the KCNE1 (G38S) polymorphism, which may be an independent risk factor for Uygur AF patients.
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The KCNQ1 F279I mutation induces a gain of function of IKs due to an impaired gating modulation of Kv7.1 induced by KCNE1, leading to a shortening of the cardiac action potential
