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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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Human Polyclonal KCNQ3 Primary Antibody for ELISA - ABIN451812
Ekberg, Schuetz, Boase, Conroy, Manning, Kumar, Poronnik, Adams: Regulation of the voltage-gated K(+) channels KCNQ2/3 and KCNQ3/5 by ubiquitination. Novel role for Nedd4-2. in The Journal of biological chemistry 2007
Chinese Hamster Polyclonal KCNQ3 Primary Antibody for WB - ABIN4893534
Ruan, Dietrich, Liu, Zimmer, Li, Singh, Zhang, Yin, Wu, Horvath, Yang: O-GlcNAc transferase enables AgRP neurons to suppress browning of white fat. in Cell 2014
In the present work, a pharmacophore-based 3D-QSAR model was generated for a series of N-pyridyl and pyrimidine benzamides possessing KCNQ2 (show KCNQ2 Antibodies)/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 (show KCNQ2 Antibodies)/Q3 opening a
Tannic acid activates Kv7.4 (show KCNQ4 Antibodies) and Kv7.3/7.5 K(+) channels resulting in vasodilation.
USP36 (show USP36 Antibodies) actions extend beyond TrkA (show NTRK1 Antibodies) because the presence of USP36 (show USP36 Antibodies) interferes with Nedd4-2 (show NEDD4L Antibodies)-dependent Kv7.2 (show KCNQ2 Antibodies)/3 channel regulation.
Carboxyl terminus helix C-D linker residues play a role in KCNQ3 current amplitudes by controlling the exit of the KCNQ3 channel from the endoplasmic reticulum.
a structural mechanism for the gating of the Kv7.3 PM and for the site of action of RTG as a Kv7.2 (show KCNQ2 Antibodies)/Kv7.3 K(+) current activator.
In bipolar disorder patients' prefrontal cortex, Kcnq3 expression was decreased, DNA methylation (show HELLS Antibodies) was decreased, and Kcnq3 mRNA was decreased compared to controls.
the clinical and EEG features of this patient further on expand the phenotypic variability of KCNQ3 gene mutations
Phosphorylation of KCNQ2 (show KCNQ2 Antibodies) and KCNQ3 anchor domains by protein kinase CK2 (show CSNK2A1 Antibodies) augments binding to AnkG (show ANK3 Antibodies).
mutations in KCNQ3, similarly to KCNQ2 (show KCNQ2 Antibodies), can be found in patients with more severe phenotypes including intellectual disability
the present results suggest that gain-of-function mutations in Kv7.2 (show KCNQ2 Antibodies)/3 currents may cause human epilepsy with a severe clinical course
KCNQ3 plays an essential role in maintaining the slow afterhyperpolarization under low phosphatidylinositol diphosphate conditions.
Mechanosensitivity of Skin Down-hair mechanoeceptors is increased in Kcnq3-/- and in Kcnq2 (show KCNQ2 Antibodies)+/-/Kcnq3-/- 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.
Data show that a reduction in Kv7.2 (show KCNQ2 Antibodies)/3 channel activity is essential for tinnitus induction and for the tinnitus-specific hyperactivity.
Retigabine is more effective on KCNQ3 than KCNQ2 (show KCNQ2 Antibodies), whereas ZnPy is more effective on KCNQ2 (show KCNQ2 Antibodies) with no detectable effect on KCNQ3.
Results show that in the same protein complex in which PKA augments L currents, AKAP79 (show AKAP5 Antibodies)/150 directs calcineurin to activate NFAT (show NFATC1 Antibodies) and initiate a longer-term feedback loop that upregulates M-channel expression, countering increased neuronal excitability.
This study demonistrated that kcnq3 gene expression in mouse dorsal raphe nucleus
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 > KCNQ4 (show KCNQ4 Antibodies) > KCNQ5 (show KCNQ5 Antibodies) > KCNQ1 (show KCNQ1 Antibodies) > KCNQ2 (show KCNQ2 Antibodies).
These findings provide novel evidence that KCNQ2 (show KCNQ2 Antibodies)/3 channels could be an important regulator in neuronal apoptosis.
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 one of two related proteins encoded by the KCNQ2 and KCNQ5 genes, 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 2 (BFNC2), also known as epilepsy, benign neonatal type 2 (EBN2). Two variants encoding distinct isoforms have been found.
potassium voltage-gated channel, KQT-like subfamily, member 3
, potassium voltage-gated channel KQT-like protein 3
, potassium voltage-gated channel subfamily KQT member 3
, potassium channel subunit alpha KvLQT3
, potassium channel, voltage-gated, subfamily Q, member 3
, voltage-gated potassium channel subunit Kv7.3
, KQT-like 3
, potassium voltage-gated channel, subfamily Q, member 3