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Human Polyclonal CHRNA4 Primary Antibody für ELISA, WB - ABIN314246
Schwarz, Schwarz, Dorigo, Stützer, Wegner, Labarca, Deshpande, Gil, Berk, Lester: Enhanced expression of hypersensitive alpha4* nAChR in adult mice increases the loss of midbrain dopaminergic neurons. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2006
Cow (Bovine) Polyclonal CHRNA4 Primary Antibody für WB - ABIN2776101
Fedi, Bach, Berkovic, Willoughby, Scheffer, Reutens: Association of a nicotinic receptor mutation with reduced height and blunted physostigmine-stimulated growth hormone release. in The Journal of clinical endocrinology and metabolism 2008
Show all 2 Pubmed References
Human Polyclonal CHRNA4 Primary Antibody für ELISA - ABIN548170
Bertrand, Picard, Le Hellard, Weiland, Favre, Phillips, Bertrand, Berkovic, Malafosse, Mulley: How mutations in the nAChRs can cause ADNFLE epilepsy. in Epilepsia 2002
and chrna4 RNAs were each expressed in a unique pattern, which changed during development
cryoelectron microscopy and the structural principles of distinct assemblies of the human alpha4beta2 nicotinic receptor
Results are comparable to the impact of nicotine on withdrawal-related impaired plasticity in smokers and suggest that alpha4beta2 nicotinic receptors are relevantly involved in plasticity deficits and restitution in smokers.
Results find that overexpression of hTau increases intracellular calcium, which in turn activates calpain-2 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
the mechanism of interaction between [Upsilon4E]GID and the agonist binding pockets of the alpha4beta2 and the halpha7 receptors, and to estimate their relative binding affinities, was investigated.
Reactive oxygen species, generated by 6-hydroxydopamine (6-OHDA), could cause the current rundown in alpha4beta2 nAChRs, which may play a role in Parkinson disease.
As well as basal forebrain and brainstem cholinergic system dysfunction, cholinergic deficits mediated through nicotinic acetylcholine receptors could be evident within key networks in AD.
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) CMPI, but not by PAM 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.
This study shows that unorthodox acetylcholine binding sites can form at the alpha5/alpha4 and beta3/alpha4 interfaces in (alpha4beta2)2alpha5 and (alpha4beta2)2beta3 nicotinic acetylcholine receptors (nAChRs) and at the alpha4/alpha5 in (beta2alpha4)2alpha5 nAChRs.
the role of CHRNA4 and CHRNA7 genetic polymorphisms in moderating auditory target and novelty attentional processing in healthy subjects exposed to the auditory "oddball" P300 paradigm.
The form containing three copies of alpha4 and two of beta2 was potentiated at low concentrations of acetylcholine chloride (ACh) and physostigmine, whereas the form containing two copies of alpha4 and three of beta2 was inhibited.
X-ray crystallographic structure of the human alpha4beta2 nicotinic receptor, the most abundant nicotinic subtype in the brain; structure provides insights into the architectural principles governing ligand recognition, heteromer assembly, ion permeation and desensitization in this prototypical receptor class
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
Prepulse inhibition may be influenced by the polymorphisms of the CHRNA4 in schizophrenia and it may be a potential endophenotype of schizophrenia.
Study observed a significant association between the rs1044396 SNP in the CHRNA4 gene and the personality trait harm avoidance
Results provide further evidence that common synonymous CHRNA4 exon 5 SNPs affect cognitive processes and suggest that they also play a role in the auditory system.
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)
Results suggest that alpha4beta2( *) nAChRs can produce sustained regulation of inhibitory post-synaptic GABA currents, in fast-spiking layer V neurons of the mouse frontal area 2.
Mice lacking alpha4 subunits in ventral midbrain consumed significantly more nicotine at the highest offered nicotine concentration compared to control mice.
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...
Results demonstrate that high-affinity alpha4beta2 nicotinic acetylcholine receptors are necessary for the effects of acute nicotine on contextual fear extinction.
Data show alpha4 subunit role in conferring potentiation by 17beta-estradiol (BEST) and indicate that the C-terminal region is involved in both binding of betaEST and potentiation, while the N-terminal domain seems involved in enhancing its efficacy.
The alpha4 nAChR subunit is regulated by protein kinase C epsilon 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
cotinine alters the assembly and trafficking of alpha4beta2 nicotinic acetylcholine receptors
The study shows that nAChR alpha4 beta2 sensitizes a MAPK-linked toxicity pathway on prolonged exposure to ABETA (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 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
Lynx1 has a role in shifting alpha4beta2 nicotinic receptor subunit stoichiometry by affecting assembly in the endoplasmic reticulum
these data indicate that a4-nAChR have an impact on motor output.
Cerebral cortex alpha4 nAChR subunits increased in rats given nicotine or varenicline, but subunits from rats given saline or saz-A during the phase 2 treatment were not significantly different from all-phase saline controls.
a new mechanism of alpha4 nAChR signaling and immune regulation in T cells, possibly accounting for the effect of smoking on the immune system.
In this study, alpha4 and alpha7 nicotinic acetylcholinesterase receptors all modulated dopamine-induced abnormal involuntary movements.
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