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anti-Human GRIA4 Antibodies:
anti-Rat (Rattus) GRIA4 Antibodies:
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Human Polyclonal GRIA4 Primary Antibody for IHC (p), IHC - ABIN314841
Earnshaw, Bressloff: Biophysical model of AMPA receptor trafficking and its regulation during long-term potentiation/long-term depression. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
Human Polyclonal GRIA4 Primary Antibody for IHC (p), WB - ABIN656865
Muntané, Horvath, Hof, Ely, Hopkins, Raghanti, Lewandowski, Wray, Sherwood: Analysis of synaptic gene expression in the neocortex of primates reveals evolutionary changes in glutamatergic neurotransmission. in Cerebral cortex (New York, N.Y. : 1991) 2015
The authors suggest that pathogenic de novo variants in GRIA4 lead to intellectual disability with or without seizures, gait abnormalities, problems of social behavior, and other variable features.
Study shows that alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluA4 is expressed on oligodendrocytes, myelin and on axons in humans.
A transient positive feedback mechanism between AMPAR and stargazin (show CACNG2 Antibodies) has implications for information processing in the brain, because it should allow activity-dependent facilitation of excitatory synaptic transmission through a postsynaptic mechanism.
This study demonstrated that the GRIA4 protein was altered in auditory cortex patient with schizophreia.
Interaction with the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluR4.
the levels were comparable for complexes containing GluR2 (show GRIA2 Antibodies), GluR3 (show GRIA3 Antibodies) and GluR4 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.
Statistical analysis showed no association between migraine and the GRIA2 (show GRIA2 Antibodies) and GRIA4 polymorphisms investigated.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA (show GRIA3 Antibodies)) receptor desensitization.
The data potentially suggest a lack of epistatic interaction between GRIA2 (show GRIA2 Antibodies) and GRIA4 variants regarding clinical outcomes in patients with major depressive disorder.
Did not observed any significant association between GRIA4 polymorphisms and clinical improvement in patients with Major depressive disorder.
These data suggest that GluA4 enables efficient homeostatic upscaling and responsiveness to temporal activity patterns during the critical period of activity-dependent refinement of the circuitry.
this study shows that curcumin increased the GluR4 expression in bone marrow-derived dendritic cells activated with lipopolysaccharides, which likely contributed to the mechanism of inhibiting the Th17 cell differentiation
GluA4 subunits are required to produce an EPSC-triggerable postsynaptic action potentials after the presynaptic action potential, while Cav3.1 (show CACNA1G Antibodies) expression is needed to establish the driver function of L5B-POm synapses at hyperpolarized membrane potentials
Data indicate that the AMPA (show GRIA3 Antibodies) receptor subunits abundance is hippocampus, GluA2 (show GRIA2 Antibodies) > GluA1 (show GRIA1 Antibodies) > GluA3 (show GRIA3 Antibodies) >> GluA4; cortex, GluA2 (show GRIA2 Antibodies) > GluA3 (show GRIA3 Antibodies) >/= GluA1 (show GRIA1 Antibodies) >> GluA4; and cerebellum, GluA2 (show GRIA2 Antibodies) > GluA3 (show GRIA3 Antibodies) >/= GluA1 (show GRIA1 Antibodies) > GluA4.
Here we identify a novel modifier - called "pecanex-like 2", or Pcnxl2 (show PCNXL2 Antibodies) for short - that reduces the severity of spike-wave dischargesin the C3H substrain in which the Gria4 mutation originally arose
GluA4 expression is sufficient to alter the signaling mechanisms of synaptic plasticity and can fully explain the switch in the kinase dependency of long-term potentiation from PKA to Ca2+/calmodulin-dependent protein kinase II (show CAMK2G Antibodies) during synapse maturation.
Postsynaptic density fractions from spinal cord dorsal horns showed an increase in GluA4 expression after morphine discontinuation.
The GluA4 subunit of the AMPA (show GRIA3 Antibodies) receptor in the hippocampus (GluA4(HC-/-) mice) was ablated, thereby selectively reducing AMPA (show GRIA3 Antibodies) receptor-mediated currents onto a subgroup of hippocampal interneurons expressing GluA4.
study found the majority of cerebellar GluA1 (show GRIA1 Antibodies)/A4-type AMPARs are expressed in Bergmann glial (BG) cells; BG AMPARs are essential to optimize synaptic integration and cerebellar output function throughout life
Western blotting of surface cross-linked cerebellar samples shows a significantly lower surface level of the GluR4 AMPA receptor subunit in Ppt1-deficient mice.
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 of this gene results in transcript variants encoding different isoforms, which may vary in their signal transduction properties. Some haplotypes of this gene show a positive association with schizophrenia.
glutamate receptor, ionotrophic, AMPA 4
, AMPA receptor GluR4/D
, glutamate receptor subunit GluR4
, glutamate receptor 4
, AMPA-selective glutamate receptor 4
, glutamate receptor, ionotropic, AMPA4 (alpha 4)
, glutamate receptor channel alpha 4
, glutamate receptor ionotropic, AMPA 4
, spike wave 1