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anti-Human GRIA4 Antibodies:
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Polyclonal GRIA4 Primary Antibody for ELISA, WB - ABIN539641
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
Show all 2 Pubmed References
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 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, GluR3 and GluR4 as well as 5-HT1A. Moreover, the levels of complexes containing muscarinic AChR M1, NR1 and GluR1 were significantly increased in male patients with AD.
Statistical analysis showed no association between migraine and the GRIA2 and GRIA4 polymorphisms investigated.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor desensitization.
The data potentially suggest a lack of epistatic interaction between GRIA2 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.
SNPs within GRIA4 may not be associated with the development and treatment outcomes in BD
No significant association GRIA4 polymorphisms was found with the diagnosis of schizophrenia.
Flip and flop splice variants of AMPA receptor subunits in the spinal cord of amyotrophic lateral sclerosis.
characterization of homomeric alpha-amino-3-hydroxy-5-methylisoxazolepropionate (AMPA)-selective GluR-D glutamate receptors carrying N-terminal deletions
Results suggest that at least one susceptibility locus for schizophrenia is located within or very close to the GRIA4 region in Japanese.
alternative splicing isoform of GluR4, human GluR4c has a 113-bp insert containing a stop codon, resulting in a short C terminus.
The minimal kinetic mechanism for channel opening is consistent with binding of two glutamate molecules per receptor complex.
GluR4 may regulate its synaptic targeting through phosphorylation-dependent interactions with alpha-Actinin-1 and IQGAP1
The present findings show that the interaction between PKCgamma and GluR4 is specifically required to assure PKC-driven phosphorylation and surface membrane expression of GluR4.
Of the three AMPA genes analyzed here, only GRIA3 seems to be involved in the pathogenesis of schizophrenia, but only in females.
The central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles are evenly distributed along the postsynaptic density. GluA4 gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 subunits are distributed at auditory nerve synapses in a target-cell-dependent manner.
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 expression is needed to establish the driver function of L5B-POm synapses at hyperpolarized membrane potentials
Data indicate that the AMPA receptor subunits abundance is hippocampus, GluA2 > GluA1 > GluA3 >> GluA4; cortex, GluA2 > GluA3 >/= GluA1 >> GluA4; and cerebellum, GluA2 > GluA3 >/= GluA1 > GluA4.
Here we identify a novel modifier - called "pecanex-like 2", or Pcnxl2 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 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 receptor in the hippocampus (GluA4(HC-/-) mice) was ablated, thereby selectively reducing AMPA receptor-mediated currents onto a subgroup of hippocampal interneurons expressing GluA4.
This study demonistrated that gira4 gene expression in mouse dorsal raphe nucleus
study found the majority of cerebellar GluA1/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.
This study suggested new moddel of absence epilepsy with gria4 deificent mice.
GluR4-deficient mice exhibit schizophrenia-related phenotypes: drastically impaired prepulse inhibition (PPI) of the acoustic startle response and enhanced sensitivity to the locomotor stimulatory effects of a NMDA receptor antagonist, MK-801.
The highest level of GluR4 mRNA was detected in rats at PND7.
These results demonstrate an essential role for Gria4 in the brain, and suggest that abnormal AMPA receptor-dependent synaptic activity can be involved in the network hypersynchrony that underlies absence seizures.
Two closely related substrains C3H/HeOuJ (OuJ) and C3H/HeSnJ, which have a similar SWD incidence as HeJ, do not contain the Gria4 mutation.
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