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anti-Human GRIA2 Anticorps:
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Mammalian Monoclonal GRIA2 Primary Antibody pour ISt, IHC - ABIN1304676
Warmus, Sekar, McCutchen, Schellenberg, Roberts, McMahon, Roberson: Tau-mediated NMDA receptor impairment underlies dysfunction of a selectively vulnerable network in a mouse model of frontotemporal dementia. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2014
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Chicken Polyclonal GRIA2 Primary Antibody pour WB - ABIN550156
Duprat, Daw, Lim, Collingridge, Isaac: GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity. dans Philosophical transactions of the Royal Society of London. Series B, Biological sciences 2003
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Mouse (Murine) Polyclonal GRIA2 Primary Antibody pour IHC (p), WB - ABIN3043838
Liu, Mei, Li, Roboti, Pang, Ying, Gao, Lowe, Bao: Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice. dans Proceedings of the National Academy of Sciences of the United States of America 2018
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Human Polyclonal GRIA2 Primary Antibody pour IHC, IHC (p) - ABIN4314579
Leja, Essaghir, Essand, Wester, Oberg, Tötterman, Lloyd, Vasmatzis, Demoulin, Giandomenico: Novel markers for enterochromaffin cells and gastrointestinal neuroendocrine carcinomas. dans Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2009
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Human Monoclonal GRIA2 Primary Antibody pour FACS, ELISA - ABIN969524
Shen, Jin: [GluR2 expression in the developing rat inferior colliculus and the relationship with development of synapse]. dans Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery 2010
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Human Polyclonal GRIA2 Primary Antibody pour CM, ICC - ABIN2746695
Puthussery, Gayet-Primo, Taylor, Haverkamp: Immunohistochemical identification and synaptic inputs to the diffuse bipolar cell type DB1 in macaque retina. dans The Journal of comparative neurology 2012
Rat (Rattus) Polyclonal GRIA2 Primary Antibody pour WB - ABIN361455
Murphy, Tcharnaia, Beshara, Jones: Cortical development of AMPA receptor trafficking proteins. dans Frontiers in molecular neuroscience 2012
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Chicken Polyclonal GRIA2 Primary Antibody pour WB - ABIN550152
Hollmann, Heinemann: Cloned glutamate receptors. dans Annual review of neuroscience 1994
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Rat (Rattus) Polyclonal GRIA2 Primary Antibody pour IP, WB - ABIN1742379
Luchkina, Huupponen, Clarke, Coleman, Keinänen, Taira, Lauri: Developmental switch in the kinase dependency of long-term potentiation depends on expression of GluA4 subunit-containing AMPA receptors. dans Proceedings of the National Academy of Sciences of the United States of America 2014
Rat (Rattus) Monoclonal GRIA2 Primary Antibody pour IP, WB - ABIN1742378
Jedlicka, Vnencak, Krueger, Jungenitz, Brose, Schwarzacher: Neuroligin-1 regulates excitatory synaptic transmission, LTP and EPSP-spike coupling in the dentate gyrus in vivo. dans Brain structure & function 2015
Study reports heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability and neurodevelopmental abnormalities. When GluA2 subunits are co-expressed with GluA1, most GRIA2 mutations cause a decreased current amplitude and some also affect voltage rectification.
Reduced expression of Gria2 increased Ca(2+) influx through Ca(2+)-permeable AMPA receptors which increased the vulnerability and affected the differentiation and migration of distinct cell populations and interfered with normal circuit formation in fragile X syndrome.
a dramatic reduction of expression of the GluA2 subunit occurs concomitantly with its hyper-phosphorylation on Serine 880 and increased ubiquitination. Consequently, Cdkl5 silencing skews the composition of membrane-inserted AMPA-Rs towards the GluA2-lacking calcium-permeable form
This review showed that the mutation GR1A protein associate with Obsessive-compulsive disorder.
Measured the expression of GRIA2 and GABRA1 in patients with methamphetamine-use disorder. Also examined whether miR-181a down-regulates GRIA2 and GABRA1 in a cell-based assay. We further examined the effects of chronic methamphetamine exposure on the expression of miR-181a, GRIA2 and GABRA1. The results demonstrated that serum GRIA2 is higher in patients with methamphetamine-use disorder than in healthy controls.
This study demonstrated that a significant decrease in the protein level of GluN2A in major depression disorder.
both the intracellular C-terminal domain (CTD) and the loop region between the M1 and M2 helices move during activation and the CTD is detached from the membrane
The results of this study suggest that neurons in hypothalamic hamartoma may bear Ca(2+) -permeable AMPA receptors(GluA2 ) due to dislocation of ADAR2
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.
The GluR2 subunit of the AMPA receptor is involved in cell migration and calcium signaling.
RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition
GRIA2*CCC polymorphism is genetic risk marker for paranoid schizophrenia in Russians.Low risk genetic markers of paranoid schizophrenia were revealed: in Tatars-GRIA2*T/T (rs43025506) of GRIA2 gene and GRIA2*CCT in Russians.
GRIA2 is a useful marker for distinguishing solitary fibrous tumour from most mimics
a link between neurodegenerative processes and deficient RNA editing of the GluA2 Q/R site.
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.
analysis of changes in receptor kinetics with the R628E charge-inverting mutation in the "linker" region of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor
We show that excitatory cortical-patterned neurons derived from multiple human pluripotent stem cell lines exhibit native-like maturation changes in AMPAR composition such that there is an increase in the expression of GluA2(R) subunits.
Studies indicate that AMPAR trafficking is a key mechanism that drives nascent synapse development, and is the main determinant of both Hebbian and homeostatic plasticity in mature synapses.
Frrsl1 deletion results in an increased proportion of immature AMPA receptors, indicated by incomplete glycosylation of GLUA2 (also known as GRIA2) and GLUA4 (also known as GRIA4) AMPA receptor proteins.
This study reveals that the C-terminal domains of GluA1 and GluA2, the key subunits of AMPARs, are necessary and sufficient to drive NMDA receptor-dependent LTP and LTD, respectively.
D2R GluA2 knockout (KO) mice showed hypoactivity, while GluA2 KO in D1R neurons had no effect on locomotor activity. D1R GluA2 KO mice showed delayed learning in the accelerating rotarod test compared with control animals, whereas D2R GluA2 KO animals exhibited complete loss of motor learning. GluA2-lacking AMPAR expression in D1R neurons induced hypersociability; D2R GluA2 KO mice elicited loss of sociability.
defects in the brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway contribute to the deregulated AMPAR trafficking.
a circuitry in which the upregulation of miR-409-3p and miR-495-3p, belonging to a brain-specific miRNA subcluster implicated in several neurodevelopmental disorders, produced the downregulation of Gria2, is reported.
GluA2 C-terminus is required for synaptic scaling in CA1 hippocampal pyramidal neurons.
translocation of surface GluA1, but not GluA2, AMPAR subunits to the synapse requires the amino-terminal domain
Critically, by altering the two interacting loops of TARP gamma2 and TARP gamma8, the authors could entirely remove all allosteric modulation of GluA2, without affecting formation of AMPA receptor-TARP complexes.
the GluA2 subunit via its interaction with GAPDH, play a critical role in cortical neurodevelopment.
The results of this study indicate that disrupting GluA2 phosphorylation leads to increased responsivity to acute stress following cocaine exposure and increased vulnerability to chronic stress.
Long-term depression proceeds upon stimulation in cerebellar Purkinje cells in mice carrying mutated GluA2 C terminus.
The data of this study indicated that GluA2-lacking AMPARs are present at D1R-expressing MSN synapses after withdrawal from both contingent and non-contingent cocaine exposure.
These data suggest that excess mu3A acts independently of the AP-3A complex to reroute AMPAR to recycling endosomes.
Topological regulation of synaptic AMPA receptor expression by the RNA-binding protein CPEB3 has been demonstrated.
Results indicate that disrupting GluA2 phosphorylation and increasing GluA2-mediated transmission in the nucleus accumbens leads to increased vulnerability to cocaine relapse.
Chronic stress-elicited depressive behavior may be due to hypertrophy of basolateral amygdala (BLA) neuronal dendrites and increased of Glur1-Glur2 ratio in BLA neurons.
found the protein levels of AMPA receptor subunits (GluR1 and GluR2) are upregulated in the amygdala and the 5-HT3 receptor is downregulated in hypothalamic regions of Socially Isolated mice.
These results provide direct evidence for cortical AMPA receptors to contribute to zymosan-induced visceral and spontaneous pain.
Animals trained in the trace fear conditioning protocol had GluA2 RNA editing levels were nearly 100% in amygdala and hippocampus.
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, GRIA1-4. The subunit encoded by this gene (GRIA2) is subject to RNA editing (CAG->CGG\; Q->R) within the second transmembrane domain, which is thought to render the channel impermeable to Ca(2+). Human and animal studies suggest that pre-mRNA editing is essential for brain function, and defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology. Alternative splicing, resulting in transcript variants encoding different isoforms, (including the flip and flop isoforms that vary in their signal transduction properties), has been noted for this gene.
AMPA-selective glutamate receptor 2
, glutamate receptor 2
, Glutamate receptor 2
, glutamate receptor ionotropic, AMPA 2
, AMPA selective glutamate receptor
, glutamate receptor B
, glutamate receptor, ionotropic, AMPA 2.1
, AMPA glutamate receptor 2
, AMPA receptor GluR2/B
, glutamate receptor AMPA 2