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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 (show MLXIP Antibodies)-330-3p up-regulated the total DNA methylation (show HELLS Antibodies) in non-small cell lung cancer cells, and co-IP-demonstrated GRIA3 was directly related with DNMT1 (show DNMT1 Antibodies) and DNMT3A (show DNMT3A Antibodies). GRIA3 is a direct target of miR (show MLXIP Antibodies)-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 (show TYR Antibodies)-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 (show GRIA2 Antibodies), GluR3 and GluR4 (show GRIA4 Antibodies) as well as 5-HT1A (show HTR1A Antibodies). Moreover, the levels of complexes containing muscarinic AChR M1, NR1 (show GRIN1 Antibodies) and GluR1 (show GRIA1 Antibodies) 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 (show GRIN1 Antibodies) 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 (show GRIA4 Antibodies) gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 (show GRIA4 Antibodies) subunits are distributed at auditory nerve synapses in a target-cell-dependent manner.
The experiments reveal a novel type of plasticity at CA1 (show CA1 Antibodies) 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 (show APP Antibodies)-mediated synaptic and cognitive deficits.
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP (show SCP2 Antibodies)), 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 (show SCP2 Antibodies) and learning are induced via cAMP-mediated Epac (show RAPGEF3 Antibodies) 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 (show GRIA2 Antibodies) > GluA1 (show GRIA1 Antibodies) > GluA3 >> GluA4 (show GRIA4 Antibodies); cortex, GluA2 (show GRIA2 Antibodies) > GluA3 >/= GluA1 (show GRIA1 Antibodies) >> GluA4 (show GRIA4 Antibodies); and cerebellum, GluA2 (show GRIA2 Antibodies) > GluA3 >/= GluA1 (show GRIA1 Antibodies) > GluA4 (show GRIA4 Antibodies).
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