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changes in methylation rates in umbilical cord samples were associated with the proportion of Firmicutes in the maternal gut (show GUSB ELISA Kits)
Novel Single Nucleotide Polymorphism at KCNQ1 implicate gene regulatory dysfunction in QT prolongation in African and Hispanic Americans.
We investigated the modification of air pollution and diabetes association by a genetic risk score covering 63 T2D genes. Five single variants near GRB14 (show GRB14 ELISA Kits), UBE2E2, PTPRD (show PTPRD ELISA Kits), VPS26A (show VPS26A ELISA Kits) and KCNQ1 showed nominally significant interactions with PM10 (P<0.05). Our results suggest that genetic risk for T2D may modify susceptibility to air pollution through alterations in insulin (show INS ELISA Kits) sensitivity.
Structural, computational, biochemical, and electrophysiological studies lead to an atomically explicit integrative structural model of the KCNE3 (show Kcne3 ELISA Kits)-KCNQ1 complex that explains how KCNE3 (show Kcne3 ELISA Kits) induces the constitutive activation of KCNQ1 channel activity, a crucial component in K(+) recycling.
in patients with type 2 diabetes, KCNQ1 rs163184 T>G variant was associated with a reduced glycaemic response to dipeptidylpeptidase-4 (show DPP4 ELISA Kits) inhibitors( DPP4I)
A small subgroup of patients with mutations on both KCNQ1 alleles and prolonged QT intervals do not present with Deafness but appear to have a similar risk of cardiac events as Jervell and Lange-Nielsen syndrome patients.
3' Untranslated region SNPs are not acting as genetic modifiers in a large group of LQT1 patients.
This study presents biallelic gene mutations in KCNQ1 in Asian Indian patients with AR JLNS (show KCNE1 ELISA Kits) and RWS. It adds to the scant worldwide literature of mutation studies in AR RWS.
Western blotting analysis combined with these pharmacological data suggest that long-term insulin (show INS ELISA Kits) treatment augments KCNQ1/KCNE1 (show KCNE1 ELISA Kits) currents by increasing KCNE1 (show KCNE1 ELISA Kits) protein expression.
The KCNQ1 gene has been also associated with Dilated cardiomyopathy in patients carrying a genetic variant that provokes a loss of function of potassium cannel or auto-immune deficiency.
the single KCNQ channel in Drosophila (dKCNQ) has similar electrophysiological properties to neuronal KCNQ2 (show KCNQ2 ELISA Kits)/3
Data show that Drosophila KCNQ (dKCNQ) is a slowly activating and slowly-deactivating K(+) current open at sub-threshold potentials that has similar properties to neuronal KCNQ2 (show KCNQ2 ELISA Kits)/3 with some features of the cardiac KCNQ1/KCNE1 (show KCNE1 ELISA Kits).
A maternal contribution of KCNQ protein and/or mRNA is essential for early embryonic development
The enhanced sensitivity of KCNQ1 gain-of-function mutations for HMR (show NR4A1 ELISA Kits)-1556 suggests the possibility of selective therapeutic targeting, and a potential proof of principle for genotype-specific treatment of this heritable arrhythmia.
There were substantial transmural gradients in Cav1.2 (show CACNA1C ELISA Kits), KChIP2 (show KCNIP2 ELISA Kits), ERG (show KCNH2 ELISA Kits), KvLQT1, Kir2.1 (show KCNJ2 ELISA Kits), NCX1 (show SLC8A1 ELISA Kits), SERCA2a (show ATP2A2 ELISA Kits) and RyR2 (show RYR2 ELISA Kits) at the mRNA and, in some cases, protein level-in every case the mRNA or protein was more abundant in the epicardium than the endocardium.
This study describes one physiological form of KCNQ1, depolarized voltage sensors with a closed pore in the absence of PIP2, and reveals a regulatory interaction between CaM and KCNQ1 that may explain CaM-mediated Long QT Syndrome.
KCNE1 (show KCNE1 ELISA Kits)/KCNQ1 was expressed in Xenopus oocytes with and without beta-catenin (show CTNNB1 ELISA Kits). Confocal microscopy revealed that beta-catenin (show CTNNB1 ELISA Kits) enhanced the KCNE1 (show KCNE1 ELISA Kits)/KCNQ1 protein abundance in the cell membrane.
results indicate that AMPK inhibits KCNQ1 activity by promoting Nedd4-2-dependent channel ubiquitination and retrieval from the plasma membrane.
S1 constrains S4 in the voltage sensor domain of Kv7.1 K+ channels
characterize a new component of the early bioelectrical circuit: the potassium channel (show KCNAB2 ELISA Kits) KCNQ1 and its accessory subunit KCNE1 (show KCNE1 ELISA Kits)
Slow delayed rectifier potassium currents mediated by mutant KCNQ1(Y111C) or KCNQ1(L114P) are paradoxically reduced by serum- and glucocorticoid-inducible kinase 1.
phenylboronic acid (PBA) activates KCNQ1/KCNE1 (show KCNE1 ELISA Kits) complexes
Collectively, the authors propose that Prmt1 (show PRMT1 ELISA Kits)-dependent facilitation of KCNQ-phosphatidylinositol-4,5-bisphosphate interaction underlies the positive regulation of KCNQ activity by arginine methylation, which may serve as a key target for prevention of neuronal hyperexcitability and seizures.
we investigated the effects of KCNQ1 A340E, a loss-of-function mutant. J343 mice bearing KCNQ1 A340E demonstrated a much higher 24-h intake of electrolytes (potassium, sodium, and chloride). KCNQ1, therefore, is suggested to play a central role in electrolyte metabolism. KCNQ1 A340E, with the loss-of-function phenotype, may dysregulate electrolyte homeostasis
The electrophysiological effects of BACE1 (show BACE ELISA Kits) on KCNQ1 reported here were independent of its enzymatic activity.
Loss of methylation at the Kcnq1 imprinted gDMD was strongly associated with trophoblast giant cell (TGC (show TGM2 ELISA Kits)) expansion.
Data show that disruption of potassium voltage-gated channel, KQT-like subfamily Q, member1 (KCNQ1) results in increased expression of cyclin-dependent kinase inhibitor 1C (Cdkn1c (show CDKN1C ELISA Kits)) only when the mutation is on the paternal allele.
S3 mutations in KCNQ1 cause diverse kinetic defects in I(Ks), affecting opening and closing properties, and can account for LQT1 (show ARFGAP1 ELISA Kits) phenotypes.
Characterization of the imprinted Kcnq1 domain which contains a differentially methylated region in intron 11 of Kcnq1.
KCNQ1, KCNE2 (show KCNE2 ELISA Kits), and SMIT1 (show SLC5A3 ELISA Kits) form reciprocally regulating complexes that affect neuronal excitability.
low expression of KCNQ1 expression was significantly associated with poor overall survival.
Which participates in the allelic repression of Kcnq1.
This gene encodes a voltage-gated potassium channel required for repolarization phase of the cardiac action potential. This protein can form heteromultimers with two other potassium channel proteins, KCNE1 and KCNE3. Mutations in this gene are associated with hereditary long QT syndrome 1 (also known as Romano-Ward syndrome), Jervell and Lange-Nielsen syndrome, and familial atrial fibrillation. This gene exhibits tissue-specific imprinting, with preferential expression from the maternal allele in some tissues, and biallelic expression in others. This gene is located in a region of chromosome 11 amongst other imprinted genes that are associated with Beckwith-Wiedemann syndrome (BWS), and itself has been shown to be disrupted by chromosomal rearrangements in patients with BWS. Alternatively spliced transcript variants have been found for this gene.
IKs producing slow voltage-gated potassium channel subunit alpha KvLQT1
, kidney and cardiac voltage dependend K+ channel
, potassium voltage-gated channel subfamily KQT member 1
, slow delayed rectifier channel subunit
, voltage-gated potassium channel subunit Kv7.1
, KCNQ-type K[+] channel
, Potassium voltage-gated channel subfamily KQT member 1
, potassium channel protein (KvLQT1)
, ventricular voltage-gated K+ channel pore-forming subunit KCNQ1
, KvLQT1 voltage-gated delayed rectifier potassium channel
, potassium voltage-gated channel, KQT-like subfamily, member 1
, potassium channel protein KCNQ1
, potassium voltage-gated channel, subfamily Q, member 1
, voltage gated potassium channel subunit
, KQT-like 1
, IKs producing slow voltage-gated potassium channel subunit alpha xKvLQT1
, Voltage-gated potassium channel subunit Kv7.1
, potassium channel protein