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Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels formed by a pentameric arrangement of alpha and beta subunits to create distinct muscle and neuronal receptors. Additionally we are shipping CHRNA2 Antibodies (31) and CHRNA2 Proteins (9) and many more products for this protein.
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Chrna2-expressing Martinotti cells selectively target L5 thick-tufted type A pyramidal cells (PCs) but not thin-tufted type B PCs.
Study described Chrna2 expression in the amygdala and propose that this expression is a marker of the medial subpallium-derived amygdala
The results of this study suggested that loss of the mouse nAChR (show CHRNA4 ELISA Kits) alpha2 subunit has very limited effects on baseline behavior but does lead to the potentiation of several nicotine-modulated behaviors.
The rare variants in CHRNA2 were significantly associated with smoking status.
a heterozygous single-nucleotide substitution in CHRNA2 gene (c.1126 C>T; p. Arg376Trp) in subjects with benign familial infantile seizures
CHRNA2 mutations play a causative role in autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE).
Results show that D478E variation in nAChR (show CHRNA4 ELISA Kits) alpha2 subunit increases the peak current responses of both alpha2beta2- and alpha2beta4-nAChRs; but the D478N variation in nAChR (show CHRNA4 ELISA Kits) alpha2 subunit only increases the peak current responses of alpha2beta2-nAChRs
Level of cigarettes per day during adolescence and young adulthood is associated with CHRNB3A6, CHRNA5A3B4, and CHRNA2
Results indicate that the CHRNA2 signal peptide mutation T22I modulates the function of both alpha2beta2- and alpha2beta4-nAChR (show CHRNA4 ELISA Kits) and decreases sensitivities to nicotine and acetylcholine, and quite possibly increasing susceptibility to nicotine dependence
findings indicate that both CHRNA2 and CHRNA6 play a significant role in the etiology of ND in AA and EA smokers
mutations of CHRNB2 (show CHRNB2 ELISA Kits) and CHRNA2 genes may be rare in Chinese autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) population.
A new CHRNA2 mutation markedly increases the receptor sensitivity to acetylcholine, indicating that the nicotinic alpha 2 subunit alteration is the underlying cause.
From a panel of 59 single-nucleotide polymorphisms (SNPs) located on 11 candidate genes, we identify four SNPs (one each on CHRNA5 (show CHRNA5 ELISA Kits) and CHRNA2 and two on CHAT) that appear to have pharmacogenetic relevance in smokin cessation therapy.
Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels formed by a pentameric arrangement of alpha and beta subunits to create distinct muscle and neuronal receptors. Neuronal receptors are found throughout the peripheral and central nervous system where they are involved in fast synaptic transmission. This gene encodes an alpha subunit that is widely expressed in the brain. The proposed structure for nAChR subunits is a conserved N-terminal extracellular domain followed by three conserved transmembrane domains, a variable cytoplasmic loop, a fourth conserved transmembrane domain, and a short C-terminal extracellular region. Mutations in this gene cause autosomal dominant nocturnal frontal lobe epilepsy type 4. Single nucleotide polymorphisms (SNPs) in this gene have been associated with nicotine dependence.
cholinergic receptor, nicotinic, alpha 2 (neuronal)
, alpha-2 subunit, nicotinic acetylcholine receptor
, cholinergic receptor, nicotinic, alpha polypeptide 2 (neuronal)
, neuronal acetylcholine receptor subunit alpha-2
, cholinergic receptor, nicotinic, alpha polypeptide 2a
, nicotinic acetylcholine receptor
, neuronal acetylcholine receptor subunit alpha-2-like
, acetylcholine receptor, nicotinic, alpha 2 (neuronal)