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anti-Human KCNQ1 Antibodies:
anti-Rat (Rattus) KCNQ1 Antibodies:
anti-Mouse (Murine) KCNQ1 Antibodies:
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Mammalian Monoclonal KCNQ1 Primary Antibody for ISt, IHC - ABIN1304774
Salomonsson, Brasen, Braunstein, Hagelqvist, Holstein-Rathlou, Sorensen: K(V)7.4 channels participate in the control of rodent renal vascular resting tone. in Acta physiologica (Oxford, England) 2015
Show all 5 Pubmed References
Human Polyclonal KCNQ1 Primary Antibody for ELISA, WB - ABIN451757
Yasuda, Miyake, Horikawa, Hara, Osawa, Furuta, Hirota, Mori, Jonsson, Sato, Yamagata, Hinokio, Wang, Tanahashi, Nakamura, Oka, Iwasaki, Iwamoto, Yamada, Seino, Maegawa, Kashiwagi, Takeda, Maeda, Shin et al.: Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus. ... in Nature genetics 2009
Cow (Bovine) Polyclonal KCNQ1 Primary Antibody for IHC, WB - ABIN2776085
Zhou, Tan, Paz, Ogawa, Chou, Hayashi, Nihei, Fishbein, Chen, Lin, Chen: Antiarrhythmic effects of beta3-adrenergic receptor stimulation in a canine model of ventricular tachycardia. in Heart rhythm : the official journal of the Heart Rhythm Society 2008
Human Monoclonal KCNQ1 Primary Antibody for FACS, ELISA - ABIN969227
Jiang, Xu, Wang, Toyoda, Liu, Zhang, Robinson, Tseng: Dynamic partnership between KCNQ1 and KCNE1 and influence on cardiac IKs current amplitude by KCNE2. in The Journal of biological chemistry 2009
Dog (Canine) Polyclonal KCNQ1 Primary Antibody for IF (p), IHC (p) - ABIN721015
Zhao, Xu, Yun, Zhao, Li, Gong, Yuan, Yan, Zhang, Ding, Wang, Zhang, Dong, Xiu, Yang, Liu, Xue, Li: Chronic obstructive sleep apnea causes atrial remodeling in canines: mechanisms and implications. in Basic research in cardiology 2014
A novel homozygous KCNQ1 frameshift mutation, c.1426_1429delATGC (M476Pfs*4), was identified, and then the current literatures of five patients were reviewed regarding the Long QT syndrome.
The study demonstrated an increased rare variants burden for 54 genes associated with platelet function, and identified a putative role for rare damaging variants in the KCNQ1 gene on LVIS susceptibility in the Polish population.
Effect of KCNQ1 G229D mutation on cardiac pumping efficacy and reentrant dynamics in ventricles.
KCNQ1-R562S mutation reduces effective IKs due to channel gating alteration with a mild clinical expression in the heterozygous state due to minimal dominant phenotype. In the homozygous state, it is exhibited with a moderately severe Romano-Ward Long QT Syndrome phenotype due to the incomplete absence of IKs.
his study further substantiates a causal link between the V307L KCNQ1 mutation and pro-arrhythmia in human ventricles
The results of the study showed that there were significant differences in the allele frequencies of between KCNQ1 rs2283228 allele of C and rs2237896 in the Turkish Cypriot population.
The possible pathway in which KCNQ1 gene affects MetS.
Evidence indicates that genetic and epigenetic determinants at the KCNQ1 locus influence insulin sensitivity.
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.
We identified complex aberrant messenger RNA variants in the A344Aspl hiPSC-CM model and successfully recapitulated the clinical phenotypes of the patient with concealed LQT1.
KCNQ1p.Thr312del induces a loss of function in channel electrophysiology, and it is a high-risk mutation responsible for LQT1.
Long QT syndrome type 1 patients carrying the KCNQ1 D317N mutation were at higher risk for cardiac events before initiation of beta-blocker.
The exon sequencing results of KCNQ1 gene in 2 Xinjiang Uygur congenital long LQT1 families showed that exon16 missense changes (133G to A (G45S)) can lead to amino acid mutation, this mutation may be a pathogenic mutation.
Polymorphisms in KCNQ1 is associated with Polycystic ovary syndrome and type-2 diabetes.
KCNQ1 genetic variants might be associated with hypertension in individuals with type 2 diabetes mellitus.
DNA hypermethylation of KCNQ1 promoter resulted in its downregulation in hepatocellular carcinoma (HCC). Bioinformatic analysis indicated a regulatory role of KCNQ1 in the epithelial-to-mesenchymal transition process. Gain-of-function study showed that KCNQ1 exhibited remarkable inhibitory roles on tumor metastasis in vitro and in vivo.
Two voltage-gated K+ channel KCNQ1 (KCNQ1) gain-of-function mutations that cause a genetic form of atrial fibrillation, S140G and V141M, drastically slow IKs deactivation.
There was no significant difference in current density between heterozygous KCNQ1-F127L, -P477L, or -L619M variant-containing channels compared to KCNQ1-WT.
novel variants in SCN5A, KCNH2 and KCNQ1 are associated with congenital long QT syndrome in a Polish population
inactivation of KCNQ1 channels derives from the different mechanisms of the voltage sensor domain-pore coupling that lead to the intermediate open (IO) and activated open (AO) states
the single KCNQ channel in Drosophila (dKCNQ) has similar electrophysiological properties to neuronal KCNQ2/3
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 KCNQ2/3 with some features of the cardiac KCNQ1/KCNE1.
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-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/KCNQ1 was expressed in Xenopus oocytes with and without beta-catenin. Confocal microscopy revealed that beta-catenin enhanced the KCNE1/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 KCNQ1 and its accessory subunit KCNE1
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 complexes
PKCepsilon isoenzyme mediates the inhibitory action of Angiotensin II on slowly activating delayed rectifier K(+) curren and by phosphorylating distinct sites in KCNQ1/KCNE1, cPKC and PKCepsilon isoenzymes produce the contrary regulatory effects on the channel.
A double mutant mouse lacking both KCNQ1-KCNE3 and TASK-2 showed a much reduced cAMP-mediated anion secretion compared to that observed in the single KCNQ1-KCNE3 deficient mouse.
KCNQ activation decreased seizure latency by >/=50% in Kcnq1 strain mice but had no effect in the Kcna1 strain. However, in simultaneous EEG and ECG recordings, KCNQ activation significantly reduced spontaneous seizure frequency in Kcna1-/- mice by ~60%. In Kcnq1 mice, KCNQ activation produced adverse cardiac effects including profound bradycardia and abnormal increases in heart rate variability and AV conduction blocks.
Our data indicate that mouse embryonic stem cells are induced into islet-like cells in vitro. The gene imprinting status of Kcnq1 and Cdkn1c may be changed in differentiated cells during the induction in vitro.
SUMOylation of KCNQ1 is KCNE1 dependent and determines the native attributes of cardiac IKs in vivo.
Collectively, the authors propose that Prmt1-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 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) 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) 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 phenotypes.
Characterization of the imprinted Kcnq1 domain which contains a differentially methylated region in intron 11 of Kcnq1.
KCNQ1, KCNE2, and SMIT1 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.
H(+)-K(+)-ATPase/KCNQ1 reside in independent intracytoplasmic membrane compartments, or membrane domains, and upon activation of parietal cells, both membrane proteins are transported, possibly via Rab11-positive recycling endosomes, to apical membranes.
our studies reveal regulatory mechanisms within the Kcnq1 imprinted domain that operate exclusively in the heart on Kcnq1 a gene crucial for heart development and function.
KCNE2 influences blood-CSF anion flux by regulating KCNQ1 and KCNA3 in the choroid plexus epithelium.
Expression of KCNQ1 and NKCC1 protein in the stria vascularis of C57BL/6J mice decreases with age.
may serve as an important compensatory mechanism to protect against arrhythmias such as torsades de pointes
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