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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 Proteins (5) and many more products for this protein.
Showing 10 out of 84 products:
Chicken Polyclonal KCNQ2 Primary Antibody for 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 references for ABIN2776304
Hamster Monoclonal KCNQ2 Primary Antibody for ICC, IF - ABIN2482772
Wuttke, Penzien, Fauler, Seebohm, Lehmann-Horn, Lerche, Jurkat-Rott: Neutralization of a negative charge in the S1-S2 region of the KV7.2 (KCNQ2) channel affects voltage-dependent activation in neonatal epilepsy. in The Journal of physiology 2008
Chicken Polyclonal KCNQ2 Primary Antibody for IHC, WB - ABIN2776302
Etxeberria, Aivar, Rodriguez-Alfaro, Alaimo, Villacé, Gómez-Posada, Areso, Villarroel: Calmodulin regulates the trafficking of KCNQ2 potassium channels. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2008
Chicken Polyclonal KCNQ2 Primary Antibody for IHC, WB - ABIN2776303
Soldovieri, Castaldo, Iodice, Miceli, Barrese, Bellini, Miraglia del Giudice, Pascotto, Bonatti, Annunziato, Taglialatela: Decreased subunit stability as a novel mechanism for potassium current impairment by a KCNQ2 C terminus mutation causing benign familial neonatal convulsions. in The Journal of biological chemistry 2006
The KCNQ2 and KCNQ3 (show KCNQ3 Antibodies) 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 (show KCNQ3 Antibodies) PM and for the site of action of RTG as a Kv7.2/Kv7.3 (show KCNQ3 Antibodies) 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 Antibodies)-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 Antibodies) 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 (show KCNQ3 Antibodies) anchor domains by protein kinase CK2 (show CSNK2A1 Antibodies) augments binding to AnkG (show ANK3 Antibodies).
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 (show KCNQ3 Antibodies)-/- and in Kcnq2+/-/Kcnq3 (show KCNQ3 Antibodies)-/- 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 (show KCNQ3 Antibodies) than KCNQ2, whereas ZnPy is more effective on KCNQ2 with no detectable effect on KCNQ3 (show KCNQ3 Antibodies).
Results show that in the same protein complex in which PKA augments L currents, AKAP79 (show AKAP5 Antibodies)/150 directs calcineurin (show PPP3CA Antibodies) to activate NFAT (show NFATC1 Antibodies) 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 (show KCNQ3 Antibodies) > KCNQ4 (show KCNQ4 Antibodies) > KCNQ5 (show KCNQ5 Antibodies) > KCNQ1 (show KCNQ1 Antibodies) > 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