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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
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
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
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
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
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
Results reveal a role for the KCNQ1 potassium channel in the regulation of growth, and show that growth hormone deficiency associated with maternally inherited gingival fibromatosis is an allelic disorder with cardiac arrhythmia syndromes caused by KCNQ1 mutations.
The conservation of homologous residues in helix B of other Kv7 subtypes confer similar competition of Ca(2+)-calmodulin (CaM) with PIP2 binding to their proximal C-termini and suggest that PIP2-CaM interactions converge to Kv7 helix B to modulates channel activity in a Kv7 subtype-dependent manner.
expression of the nearby cyclindependent kinase inhibitor 1C (CDKN1C) gene was revealed to be upregulated after SP3 knockdown in cells that possessed non-risk alleles. This suggests that CDKN1C is potentially one of the functional targets of SNP rs163184, which modulates the binding activity of the locus for Sp3 and Lsd1/Kdm1a
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.
Electron Microscopy of Full-Length alpha-Subunit of Human Potassium Channel Kv7.1
Predicting the Functional Impact of KCNQ1 Variants of Unknown Significance
Low KCNQ1 expression is associated with colorectal cancer.
SUMOylation of KCNQ1 is KCNE1 dependent and determines the native attributes of cardiac IKs in vivo.
these data strongly suggest that KCNQ1 genetic polymorphism influences repaglinide response due to the pivotal role of KCNQ1 in regulating insulin resistance through the IRS-2/PI(3)K/Akt signaling pathway.
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-mediated regulation of the voltage dependence of activation of the KV7.1 channel.
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.
findings presented here will have some implications in understanding the potential off-target interactions of the drugs with the KCNQ1/KCNE1 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
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
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.
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.
We showed the disturbance of parietal cell differentiation and mucous neck-to-zymogenic cell lineage differentiation with enhanced expression of KCNQ1 in the parietal cells.
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 > KCNQ4 > KCNQ5 > KCNQ1 > KCNQ2.
These results suggest that increased KCNQ1 protein expression limits insulin secretion from pancreatic beta-cells by regulating the potassium channel current.
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