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The M channel is a slowly activating and deactivating potassium channel that plays a critical role in the regulation of neuronal excitability.
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Mammalian Monoclonal KCNQ2 Primary Antibody pour ISt, IHC - ABIN1304776
Miceli, Soldovieri, Ambrosino, De Maria, Migliore, Migliore, Taglialatela: Early-onset epileptic encephalopathy caused by gain-of-function mutations in the voltage sensor of Kv7.2 and Kv7.3 potassium channel subunits. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
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Cow (Bovine) Polyclonal KCNQ2 Primary Antibody pour IHC, WB - ABIN2776304
Tang, Li, Xia, Jiang, Pan, Shen, Long, Zhao, Cai: A novel mutation in KCNQ2 gene causes benign familial neonatal convulsions in a Chinese family. dans Journal of the neurological sciences 2004
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The KCNQ2 and KCNQ3 (Montrer KCNQ3 Anticorps) genes are located on the terminal region of chromosomes 22 and 9, respectively. The KCNQ2 gene tree exhibited close clustering between horses and humans, relative to horses and mice.
patients with the KCNQ2 E515D mutation are susceptible to seizures.
he present study involves identification of newer anti-epileptic agents by means of a computer-aided drug design adaptive protocol involving both structure-based virtual screening of Asinex library using homology model of KCNQ2 and 3D-QSAR based virtual screening with docking analysis, followed by dG bind and ligand efficiency calculations with ADMET studies, of which 20 hits qualified all the criterions.
This study provided evidence to suggests that the p.R213Q mutation has a dominant-negative effect on the current amplitude of homomeric wild-type and mutant KCNQ2 constructs, which correlates with clinical seizure frequencies and neurodevelopmental outcomes.
Mutations in STXBP1 (Montrer STXBP1 Anticorps) encoding the syntaxin binding protein 1 (Montrer STXBP1 Anticorps) can produce a phenotype similar to that of KCNQ2 mutations
whole exome sequencing in families with ID and history of autosomal dominant inheritance pattern with or without seizures, may further broaden the phenotypic spectrum of KCNQ2 associated epileptic encephalopathy or encephalopathy
The direct effect of heat on KCNQ2 channels may be involved in excitability regulation of neurons, and the P-loop region is critical for temperature-dependent modulation of the expression and trafficking of KCNQ2 channels.
Epileptic encephalopathy with burst suppression without brain malformations is associated with pathogenic variation in KCNQ2.
Heterozygous KCNQ2 R201C and R201H gain-of-function variants present with profound neonatal encephalopathy in the absence of neonatal seizures.
This study provide evidence for a new phenotypic and functional profile in KCNQ2-related epilepsy.
In the present work, a pharmacophore-based 3D-QSAR model was generated for a series of N-pyridyl and pyrimidine benzamides possessing KCNQ2/Q3 opening activity. The pharmacophore model generated contains one hydrogen bond donor (D), one hydrophobic (H), and two aromatic rings (R). They are the crucial molecular write-up detailing predicted binding efficacy of high affinity and low affinity ligands for KCNQ2/Q3 opening a
The data of this study showed that, in Kcnq2 mutant slices, burst activity was modulated by GABAA (Montrer GABRg1 Anticorps) receptor blockade.
Kcnq2 ablation leads to increased neuronal excitability of neocortex layer 2/3 pyramidal neurons.
USP36 (Montrer USP36 Anticorps) actions extend beyond TrkA (Montrer NTRK1 Anticorps) because the presence of USP36 (Montrer USP36 Anticorps) interferes with Nedd4-2 (Montrer NEDD4L Anticorps)-dependent Kv7.2/3 channel regulation.
Mechanosensitivity of Skin Down-hair mechanoeceptors is increased in Kcnq3 (Montrer KCNQ3 Anticorps)-/- and in Kcnq2+/-/Kcnq3 (Montrer KCNQ3 Anticorps)-/- Mutant Mice.
Resilience to tinnitus is developed in mice that show a re-emergence of KCNQ2/3 channel activity and a reduction in HCN channel activity.
Reduced M-current in the superior cervical ganglion neurons of Kcnq2 truncation mutation heterozygotic mice.
Data show that a reduction in Kv7.2/3 channel activity is essential for tinnitus induction and for the tinnitus-specific hyperactivity.
Retigabine is more effective on KCNQ3 (Montrer KCNQ3 Anticorps) than KCNQ2, whereas ZnPy is more effective on KCNQ2 with no detectable effect on KCNQ3 (Montrer KCNQ3 Anticorps).
Results show that in the same protein complex in which PKA augments L currents, AKAP79 (Montrer AKAP5 Anticorps)/150 directs calcineurin to activate NFAT (Montrer NFATC1 Anticorps) and initiate a longer-term feedback loop that upregulates M-channel expression, countering increased neuronal excitability.
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 (Montrer KCNQ3 Anticorps) > KCNQ4 (Montrer KCNQ4 Anticorps) > KCNQ5 (Montrer KCNQ5 Anticorps) > KCNQ1 (Montrer KCNQ1 Anticorps) > KCNQ2.
The M channel is a slowly activating and deactivating potassium channel that plays a critical role in the regulation of neuronal excitability. The M channel is formed by the association of the protein encoded by this gene and a related protein encoded by the KCNQ3 gene, both integral membrane proteins. M channel currents are inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. Defects in this gene are a cause of benign familial neonatal convulsions type 1 (BFNC), also known as epilepsy, benign neonatal type 1 (EBN1). At least five transcript variants encoding five different isoforms have been found for this gene.
, neuroblastoma-specific potassium channel protein
, neuroblastoma-specific potassium channel subunit alpha KvLQT2
, potassium voltage-gated channel subfamily KQT member 2
, voltage-gated potassium channel subunit Kv7.2
, potassium channel subunit alpha KvLQT2
, potassium voltage-gated channel, subfamily Q, member 2