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and chrna4 RNAs were each expressed in a unique pattern, which changed during development
Results find that overexpression of hTau increases intracellular calcium, which in turn activates calpain-2 (show CAPN2 Proteins) and induces degradation of alpha4 nAChR.
Orienting attention predicted by CHRNA4 and maternal sensitivity interaction in 6-month-old infants.
This study demonstrated that rs1044396 of CHRNA4 was significantly associated with Internet gaming disorder
A polymorphism in CHRNA4 leads to an overdominant effect at this locus, with higher activity in the cingulo-opercular network underlying alertness.
Ability to navigate in the wilderness benefits from heightened ability to focus attention (CHRNA4).
Data suggest that amino acid residues alpha4Gly-41, alpha4Lys-64, and alpha4Thr-66 are critical for (alpha4)3(beta2)2 neuronal AChR potentiation by positive allosteric modulator (PAM (show PAM Proteins)) CMPI, but not by PAM (show PAM Proteins) NS9283; amino acid substitution at alpha4His-116, a known determinant of NS9283 binding and of agonist binding at alpha4:alpha4 subunit interface, did not reduce CMPI potentiation.
the role of CHRNA4 and CHRNA7 (show CHRNA7 Proteins) genetic polymorphisms in moderating auditory target and novelty attentional processing in healthy subjects exposed to the auditory "oddball" P300 (show EP300 Proteins) paradigm.
The form containing three copies of alpha4 and two of beta2 was potentiated at low concentrations of acetylcholine chloride (ACh (show FGFR3 Proteins)) and physostigmine, whereas the form containing two copies of alpha4 and three of beta2 was inhibited.
findings indicate that alterations in expression of the alpha4beta2 subtype of nAChR may be involved in the molecular mechanism(s) underlying the cognitive deficit associated with vascular dementia
Study presented several lines of evidence for the role of a variant encoding CHRNA4 R336C in smoking behavior and risk of smoking-related diseases
Data suggest that receptor complex assembly from Chrna4 and Chrnb2 on neuronal cell surface is up-regulated by nicotine; combined effects of increased assembly stoichiometry and preferential trafficking likely drive up-regulation of this receptor complex on neuronal cell surface upon nicotine exposure. (Chrna4 = a4 nicotinic receptor; Chrnb2 = b2 nicotinic receptor)
Varenicline treatment may prevent scopolamine-induced memory disturbance by a molecular mechanism that may involve increased alpha4beta2 nAChR availability. Varenicline dose-dependently increased protein expression of both the alpha4 and beta2 subunit in cell cultures and brain tissues, respectively, but had no effect on mRNA expression; lack of change in mRNA expression suggests a still unknown post-transcriptional me...
The alpha4 nAChR subunit is regulated by protein kinase C epsilon (show PRKCE Proteins) phosphorylation.
neuroinflammation is sufficient to provoke the decrease of a7 and a4b2 nAChRs, Ab42 accumulation and memory impairment in mice and a7(1-208) nAChR-specific antibodies can cause inflammation of the brain with symptoms typical for Alzheimer disease.
Lynx2 and Ly6g6e have roles in intracellular trafficking and allosteric potentiation of alpha4beta2 nAChRs, respectively
The study shows that nAChR alpha4 beta2 sensitizes a MAPK (show MAPK1 Proteins)-linked toxicity pathway on prolonged exposure to ABETA (show APP Proteins) (1-42).
This study has revealed complex effects of Chrna4 deficiency and prenatal nicotine exposure on ventilatory and metabolic interactions and responses to stress.
It indicated that Correlation between nAChalpha4-, 5-HT1A- and 5-HT7-containing receptors and latencies on day 16 may point to a probable link in extinction mechanisms.
These results question the conclusion that a dominant-negative mechanism would explain the dominance of the mutant L501fsX533 Fz4 (show FZD4 Proteins) allele in the transmission of a form of Familial exudative vitreoretinopathy.
Study demonstrates that chronic pre-exposure to nicotine at a dosing regimen that results in maximal alpha4 nAChR upregulation results in significantly elevated oral nicotine self-administration in a two-bottle choice paradigm in mice
This gene encodes a nicotinic acetylcholine receptor, which belongs to a superfamily of ligand-gated ion channels that play a role in fast signal transmission at synapses. These pentameric receptors can bind acetylcholine, which causes an extensive change in conformation that leads to the opening of an ion-conducting channel across the plasma membrane. This protein is an integral membrane receptor subunit that can interact with either nAChR beta-2 or nAChR beta-4 to form a functional receptor. Mutations in this gene cause nocturnal frontal lobe epilepsy type 1. Polymorphisms in this gene that provide protection against nicotine addiction have been described. Alternative splicing results in multiple transcript variants.
neuronal acetylcholine receptor subunit alpha-4
, Neuronal acetylcholine receptor subunit alpha-4-like
, cholinergic receptor, nicotinic, alpha 4
, neuronal acetylcholine receptor subunit alpha-4-like
, neuronal nicotinic acetylcholine receptor alpha 4 subunit
, alpha-4 subunit, nicotinic acetylcholine receptor
, cholinergic receptor, nicotinic, alpha polypeptide 4
, neuronal nicotinic acetylcholine receptor alpha-4 subunit
, Neuronal nicotinic acetylcholine receptor alpha 4 subunit
, cholinergic receptor, nicotinic, alpha 4 subunit
, neuronal acetylcholine receptor alpha-4 subunit
, a4 nicotinic receptor
, acetylcholine receptor alpha 4 neural
, acetylcholine receptor, neuronal, nicotinic, alpha-4 subunit
, alpha4 nAChR