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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. Additionally we are shipping Potassium Voltage-Gated Channel, KQT-Like Subfamily, Member 2 Antibodies (87) and many more products for this protein.
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The KCNQ2 and KCNQ3 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.
a structural mechanism for the gating of the Kv7.3 PM and for the site of action of RTG as a Kv7.2/Kv7.3 K(+) current activator.
There is a variable clinical expression in infantile epilepsy patients with mosaicism for KCNQ2 mutations.
Our data indicate that the TW site is dispensable for function, contributes to the stabilization of the CaM (show CALM1 Proteins)-Kv7.2 complex and becomes essential when docking to either helix A or when helix B is perturbed.
all the patients carrying the p.A294V mutation of KCNQ2 presented the clinical and EEG characteristics of early onset epileptic encephalopathy
Kcnq2 protein and mRNA expression and DNA methylation (show HELLS Proteins) status did not differ significantly between bipolar disorder patients and controls.
A novel and rare mutation was identified in KCNQ2 and was likely responsible for the benign seizures.
Phosphorylation of KCNQ2 and KCNQ3 anchor domains by protein kinase CK2 augments binding to AnkG.
The results of thus study suggested that the type of KCNQ2 mutation might influence Antiepileptic drug response epilepsy as well as developmental outcome.
Epileptic encephalopathy related to mutations in the KCNQ2 genes.
Collectively, this work reveals that residue C106 in S1 can be very close to several N-terminal S4 residues for stabilizing different KCNQ2 resting conformations.
Mechanosensitivity of Skin Down-hair mechanoeceptors is increased in Kcnq3-/- and in Kcnq2+/-/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.
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 than KCNQ2, whereas ZnPy is more effective on KCNQ2 with no detectable effect on KCNQ3.
Results show that in the same protein complex in which PKA augments L currents, AKAP79 (show AKAP5 Proteins)/150 directs calcineurin (show PPP3CA Proteins) to activate NFAT (show NFATC1 Proteins) 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 > KCNQ4 (show KCNQ4 Proteins) > KCNQ5 (show KCNQ5 Proteins) > KCNQ1 (show KCNQ1 Proteins) > KCNQ2.
These findings provide novel evidence that KCNQ2/3 channels could be an important regulator in neuronal apoptosis.
These findings demonstrate that spectrin cytoskeleton finely regulates ion channel distribution and implicates KCNQ2/3 subunits in axonal excitability and in myokymia etiology.
Suppression of neuronal KCNQ2 current in mice is associated with spontaneous seizures, behavioral hyperactivity and morphological changes in hippocampus.
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