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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. Zusätzlich bieten wir Ihnen und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 51 products:
Human Polyclonal KCNQ3 Primary Antibody für 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 für 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 (zeige KCNQ2 Antikörper)/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 (zeige KCNQ2 Antikörper)/Q3 opening a
Tannic acid activates Kv7.4 (zeige KCNQ4 Antikörper) and Kv7.3/7.5 K(+) channels resulting in vasodilation.
USP36 (zeige USP36 Antikörper) actions extend beyond TrkA (zeige NTRK1 Antikörper) because the presence of USP36 (zeige USP36 Antikörper) interferes with Nedd4-2 (zeige NEDD4L Antikörper)-dependent Kv7.2 (zeige KCNQ2 Antikörper)/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 (zeige KCNQ2 Antikörper)/Kv7.3 K(+) current activator.
In bipolar disorder patients' prefrontal cortex, Kcnq3 expression was decreased, DNA methylation (zeige HELLS Antikörper) 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 (zeige KCNQ2 Antikörper) and KCNQ3 anchor domains by protein kinase CK2 (zeige CSNK2A1 Antikörper) augments binding to AnkG (zeige ANK3 Antikörper).
mutations in KCNQ3, similarly to KCNQ2 (zeige KCNQ2 Antikörper), can be found in patients with more severe phenotypes including intellectual disability
the present results suggest that gain-of-function mutations in Kv7.2 (zeige KCNQ2 Antikörper)/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 (zeige KCNQ2 Antikörper)+/-/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 (zeige KCNQ2 Antikörper)/3 channel activity is essential for tinnitus induction and for the tinnitus-specific hyperactivity.
Retigabine is more effective on KCNQ3 than KCNQ2 (zeige KCNQ2 Antikörper), whereas ZnPy is more effective on KCNQ2 (zeige KCNQ2 Antikörper) with no detectable effect on KCNQ3.
Results show that in the same protein complex in which PKA augments L currents, AKAP79 (zeige AKAP5 Antikörper)/150 directs calcineurin to activate NFAT (zeige NFATC1 Antikörper) 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 (zeige KCNQ4 Antikörper) > KCNQ5 (zeige KCNQ5 Antikörper) > KCNQ1 (zeige KCNQ1 Antikörper) > KCNQ2 (zeige KCNQ2 Antikörper).
These findings provide novel evidence that KCNQ2 (zeige KCNQ2 Antikörper)/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