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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 Potassium Voltage-Gated Channel, KQT-Like Subfamily, Member 2 Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 92 products:
Mammalian Monoclonal KCNQ2 Primary Antibody für 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. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
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Cow (Bovine) Polyclonal KCNQ2 Primary Antibody für 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. in Journal of the neurological sciences 2004
Show all 3 Pubmed References
The KCNQ2 and KCNQ3 (zeige KCNQ3 Antikörper) 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.
Mutations in STXBP1 (zeige STXBP1 Antikörper) encoding the syntaxin binding protein 1 (zeige STXBP1 Antikörper) 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
This study demonstrated that Mutations in the KCNQ2 gene encoding the voltage-gated potassium channel subunit Kv7.2 cause early onset epileptic encephalopathy .
This work shows for the first time the association between KCNQ2 mutations and startle attacks in 38% of patients, which opens the possibility to define electroclinical phenotypes associated to KCNQ2 mutations. It also demonstrates that KCNQ2 mutations contribute to an important percentage of Spanish patients with epilepsy.
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 Kv7.2/3 channel regulation.
The data of this study showed that, in Kcnq2 mutant slices, burst activity was modulated by GABAA (zeige GABRg1 Antikörper) receptor blockade.
Kcnq2 ablation leads to increased neuronal excitability of neocortex layer 2/3 pyramidal neurons.
Mechanosensitivity of Skin Down-hair mechanoeceptors is increased in Kcnq3 (zeige KCNQ3 Antikörper)-/- and in Kcnq2+/-/Kcnq3 (zeige KCNQ3 Antikörper)-/- 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 (zeige KCNQ3 Antikörper) than KCNQ2, whereas ZnPy is more effective on KCNQ2 with no detectable effect on KCNQ3 (zeige KCNQ3 Antikörper).
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.
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 (zeige KCNQ3 Antikörper) > KCNQ4 (zeige KCNQ4 Antikörper) > KCNQ5 (zeige KCNQ5 Antikörper) > KCNQ1 (zeige KCNQ1 Antikörper) > 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