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抗Rat (Rattus) Glutamate Receptor 3 抗体:
抗Human Glutamate Receptor 3 抗体:
抗Mouse (Murine) Glutamate Receptor 3 抗体:
Human Monoclonal Glutamate Receptor 3 Primary Antibody for IHC, ELISA - ABIN969177
Utge, Soronen, Partonen, Loukola, Kronholm, Pirkola, Nyman, Porkka-Heiskanen, Paunio: A population-based association study of candidate genes for depression and sleep disturbance. in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 2010
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Human Monoclonal Glutamate Receptor 3 Primary Antibody for IHC, ELISA - ABIN966225
Am: Trust in Nanotechnology? On Trust as Analytical Tool in Social Research on Emerging Technologies. in Nanoethics 2011
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Results suggest a role for GluA3 channel activity in the regulation of sleep behavior in both mice and humans.
miR (显示 MLXIP 抗体)-330-3p up-regulated the total DNA methylation (显示 HELLS 抗体) in non-small cell lung cancer cells, and co-IP-demonstrated GRIA3 was directly related with DNMT1 (显示 DNMT1 抗体) and DNMT3A (显示 DNMT3A 抗体). GRIA3 is a direct target of miR (显示 MLXIP 抗体)-330-3p.
This study showed the lower GluA3 mRNA levels in pregnant women.
the impaired surface expression of homomeric GluA3 receptors is caused by nonproductive assembly and aggregation to which LBD residues Tyr (显示 TYR 抗体)-454 and Arg-461 strongly contribute.
This study demonstrated that the GRIA3 protein was altered in auditory cortex patient with schizophreia.
the levels were comparable for complexes containing GluR2 (显示 GRIA2 抗体), GluR3 and GluR4 (显示 GRIA4 抗体) as well as 5-HT1A (显示 HTR1A 抗体). Moreover, the levels of complexes containing muscarinic AChR M1, NR1 (显示 GRIN1 抗体) and GluR1 (显示 GRIA1 抗体) were significantly increased in male patients with AD.
An association was observed in migraine patients with the GRIA3 single nucleotide polymorphism rs3761555.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor desensitization.
The ionotrophic glutamate (显示 GRIN1 抗体) receptors AMPA3 and AMPA3 were decreased in hippocampus in patient with multiple sclerosis.
The rs557762 and the TT haplotype in the 11th haplotype block of the GRIA3 gene were associated with feelings of guilt in females.
The central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles are evenly distributed along the postsynaptic density. GluA4 (显示 GRIA4 抗体) gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 (显示 GRIA4 抗体) subunits are distributed at auditory nerve synapses in a target-cell-dependent manner.
The experiments reveal a novel type of plasticity at CA1 (显示 CA1 抗体) hippocampal synapses that is expressed by the activation of GluA3-containing AMPARs.
GluA3 is required for normal auditory signaling, normal ultrastructure of AN-BC synapses in the cochlear nucleus and normal experience-dependent changes in auditory processing after transient sound reduction.
These experiments indicate that the presence of GluA3-containing AMPARs is critical for Abeta (显示 APP 抗体)-mediated synaptic and cognitive deficits.
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP (显示 SCP2 抗体)), but not long term depression, at parallel fiber-Purkinje cell synapses. GluA3-dependent potentiation involves a cAMP-driven change in channel conductance. GluA3-mediated LTP (显示 SCP2 抗体) and learning are induced via cAMP-mediated Epac (显示 RAPGEF3 抗体) activation.
These results provide direct evidence for cortical AMPA receptors to contribute to zymosan-induced visceral and spontaneous pain.
Data indicate that the AMPA receptor subunits abundance is hippocampus, GluA2 (显示 GRIA2 抗体) > GluA1 (显示 GRIA1 抗体) > GluA3 >> GluA4 (显示 GRIA4 抗体); cortex, GluA2 (显示 GRIA2 抗体) > GluA3 >/= GluA1 (显示 GRIA1 抗体) >> GluA4 (显示 GRIA4 抗体); and cerebellum, GluA2 (显示 GRIA2 抗体) > GluA3 >/= GluA1 (显示 GRIA1 抗体) > GluA4 (显示 GRIA4 抗体).
This study demonistrated that Gria3 gene expression in mouse dorsal raphe nucleus
This study demonistrated that the GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum.
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes composed of multiple subunits, arranged to form ligand-gated ion channels. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. The subunit encoded by this gene belongs to a family of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate)-sensitive glutamate receptors, and is subject to RNA editing (AGA->GGA\; R->G). Alternative splicing at this locus results in different isoforms, which may vary in their signal transduction properties.
glutamate receptor, ionotrophic, AMPA 3
, glutamate receptor, ionotropic, AMPA 3.2
, glutamate receptor C
, AMPA receptor GluR3/C
, glutamate receptor subunit AMPA3
, glutamate receptor 3
, AMPA GluR3
, Glutamate receptor 3-like
, glutamate receptor 3-like
, AMPA-selective glutamate receptor 3
, glutamate receptor, ionotropic, AMPA3 (alpha 3)
, glutamate receptor subunit 3
, glutamate receptor channel alpha3 subunit