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anti-Human KCNQ1 Antibodies:
anti-Rat (Rattus) 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 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
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 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
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 (show KCNAB2 Antibodies) in the regulation of growth, and show that growth hormone (show GH1 Antibodies) 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 (show CDKN1C Antibodies)) gene was revealed to be upregulated after SP3 (show SP3 Antibodies) knockdown in cells that possessed non-risk alleles. This suggests that CDKN1C (show CDKN1C Antibodies) is potentially one of the functional targets of SNP rs163184, which modulates the binding activity of the locus for Sp3 (show SP3 Antibodies) and Lsd1/Kdm1a (show KDM1A Antibodies)
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 (show KCNE1 Antibodies) beta subunits.
Electron Microscopy of Full-Length alpha-Subunit (show POLG Antibodies) of Human Potassium Channel (show KCNAB2 Antibodies) 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 (show KCNE1 Antibodies) 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 (show INS Antibodies) resistance through the IRS-2 (show IRS2 Antibodies)/PI(3 (show PI3 Antibodies))K/Akt (show AKT1 Antibodies) signaling pathway.
the single KCNQ channel in Drosophila (dKCNQ) has similar electrophysiological properties to neuronal KCNQ2 (show KCNQ2 Antibodies)/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 Antibodies)/3 with some features of the cardiac KCNQ1/KCNE1 (show KCNE1 Antibodies).
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 Antibodies)-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 Antibodies), KChIP2 (show KCNIP2 Antibodies), ERG (show KCNH2 Antibodies), KvLQT1, Kir2.1 (show KCNJ2 Antibodies), NCX1 (show SLC8A1 Antibodies), SERCA2a (show ATP2A2 Antibodies) and RyR2 (show RYR2 Antibodies) 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 Antibodies)/KCNQ1 was expressed in Xenopus oocytes with and without beta-catenin (show CTNNB1 Antibodies). Confocal microscopy revealed that beta-catenin (show CTNNB1 Antibodies) enhanced the KCNE1 (show KCNE1 Antibodies)/KCNQ1 protein abundance in the cell membrane.
results indicate that AMPK (show PRKAA2 Antibodies) inhibits KCNQ1 activity by promoting Nedd4-2 (show NEDD4L Antibodies)-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 Antibodies) KCNQ1 and its accessory subunit KCNE1 (show KCNE1 Antibodies)
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 Antibodies) complexes
Our data indicate that mouse embryonic stem cells are induced into islet-like cells in vitro. The gene imprinting status of Kcnq1 and Cdkn1c (show CDKN1C Antibodies) may be changed in differentiated cells during the induction in vitro.
Collectively, the authors propose that Prmt1 (show PRMT1 Antibodies)-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 Antibodies) 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 Antibodies)) 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 Antibodies)) 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 Antibodies) phenotypes.
Characterization of the imprinted Kcnq1 domain which contains a differentially methylated region in intron 11 of Kcnq1.
KCNQ1, KCNE2 (show KCNE2 Antibodies), and SMIT1 (show SLC5A3 Antibodies) form reciprocally regulating complexes that affect neuronal excitability.
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