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Residues K526 and K527 in Kv7.1 helix B form a critical site where CaM competes with PIP2 to stabilize the channel open state. The LQT mutant K526E revealed a severely impaired channel function with a right shift in the voltage dependence of activation, a reduced current density, and insensitivity to gating modulation by Ca(2+)-CaM.
data identify D242 aminoacidic position as a potential residue involved in the KCNE1 (zeige KCNE1 Proteine)-mediated regulation of the voltage dependence of activation of the KV7.1 channel.
Equine KV7.1/KCNE1 (zeige KCNE1 Proteine) expressed in CHO (zeige COL11A1 Proteine)-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.
findings presented here will have some implications in understanding the potential off-target interactions of the drugs with the KCNQ1/KCNE1 (zeige KCNE1 Proteine) channel that lead to cardiotoxic effects
The occurrence of KCNQ1 gene mutations in patients after MI is higher in men than in women. The presence of KCNQ1 gene mutations is not an additional risk factor for increased mortality in patients after MI.
The first evidence that synonymous variants outside the canonical splice sites in KCNQ1 can alter splicing and clinically impact phenotype.
changes in methylation rates in umbilical cord samples were associated with the proportion of Firmicutes in the maternal gut (zeige GUSB Proteine)
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 (zeige GRB14 Proteine), UBE2E2 (zeige UBE2E2 Proteine), PTPRD (zeige PTPRD Proteine), VPS26A (zeige VPS26A Proteine) 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 (zeige INS Proteine) sensitivity.
Structural, computational, biochemical, and electrophysiological studies lead to an atomically explicit integrative structural model of the KCNE3-KCNQ1 complex that explains how KCNE3 induces the constitutive activation of KCNQ1 channel activity, a crucial component in K(+) recycling.
the single KCNQ channel in Drosophila (dKCNQ) has similar electrophysiological properties to neuronal KCNQ2 (zeige KCNQ2 Proteine)/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 (zeige KCNQ2 Proteine)/3 with some features of the cardiac KCNQ1/KCNE1 (zeige KCNE1 Proteine).
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 (zeige NR4A1 Proteine)-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, KChIP2, ERG, KvLQT1, Kir2.1, NCX1, SERCA2a and RyR2 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 (zeige KCNE1 Proteine)/KCNQ1 was expressed in Xenopus oocytes with and without beta-catenin (zeige CTNNB1 Proteine). Confocal microscopy revealed that beta-catenin (zeige CTNNB1 Proteine) enhanced the KCNE1 (zeige KCNE1 Proteine)/KCNQ1 protein abundance in the cell membrane.
results indicate that AMPK (zeige PRKAA2 Proteine) inhibits KCNQ1 activity by promoting Nedd4-2 (zeige NEDD4L Proteine)-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 (zeige KCNAB2 Proteine) KCNQ1 and its accessory subunit KCNE1 (zeige KCNE1 Proteine)
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 (zeige KCNE1 Proteine) complexes
Collectively, the authors propose that Prmt1 (zeige PRMT1 Proteine)-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 (zeige BACE Proteine) 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 (zeige TGM2 Proteine)) 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 (zeige CDKN1C Proteine)) 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 (zeige ARFGAP1 Proteine) phenotypes.
Characterization of the imprinted Kcnq1 domain which contains a differentially methylated region in intron 11 of Kcnq1.
KCNQ1, KCNE2 (zeige KCNE2 Proteine), and SMIT1 (zeige SLC5A3 Proteine) 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