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anti-Human GRIA1 Anticorps:
anti-Rat (Rattus) GRIA1 Anticorps:
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Rat (Rattus) Polyclonal GRIA1 Primary Antibody pour IHC, WB - ABIN361477
Sears, Liu, Narayanan, Sharf, Yeckel, Laubach, Aghajanian, DiLeone: Regulation of nucleus accumbens activity by the hypothalamic neuropeptide melanin-concentrating hormone. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Show all 27 Pubmed References
Rat (Rattus) Polyclonal GRIA1 Primary Antibody pour WB - ABIN361476
Ferrario, Loweth, Milovanovic, Wang, Wolf: Distribution of AMPA receptor subunits and TARPs in synaptic and extrasynaptic membranes of the adult rat nucleus accumbens. dans Neuroscience letters 2011
Show all 13 Pubmed References
Mouse (Murine) Monoclonal GRIA1 Primary Antibody pour ICC, IHC - ABIN2115255
Luo, Yang, Liu, Rao, Bian, Li, Chen, Liu, Zhao, Dai, Yan, Fei et al.: Downregulation of postsynaptic density-95-interacting regulator of spine morphogenesis reduces glutamate-induced excitotoxicity by differentially regulating glutamate receptors in rat cortical ... dans The FEBS journal 2013
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Rat (Rattus) Polyclonal GRIA1 Primary Antibody pour WB - ABIN3044451
Zhong, Han, Qiu, Lu, Chen, Chen, Hei, Mi: A comparison of the proliferative capacity and ultrastructure of proliferative cells from the cochleae of newborn rats of different ages. dans International journal of pediatric otorhinolaryngology 2010
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Dog (Canine) Polyclonal GRIA1 Primary Antibody pour WB - ABIN550185
Roche, OBrien, Mammen, Bernhardt, Huganir: Characterization of multiple phosphorylation sites on the AMPA receptor GluR1 subunit. dans Neuron 1996
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Human Polyclonal GRIA1 Primary Antibody pour WB - ABIN550186
Mammen, Kameyama, Roche, Huganir: Phosphorylation of the alpha-amino-3-hydroxy-5-methylisoxazole4-propionic acid receptor GluR1 subunit by calcium/calmodulin-dependent kinase II. dans The Journal of biological chemistry 1998
Show all 3 Pubmed References
Human Polyclonal GRIA1 Primary Antibody pour IHC, WB - ABIN3015589
Liu, Feng, Chen, Luo, Yan, Chen, Lin, Ding, Wen: Dcf1 Triggers Dendritic Spine Formation and Facilitates Memory Acquisition. dans Molecular neurobiology 2018
Human Polyclonal GRIA1 Primary Antibody pour IHC (p), WB - ABIN3043837
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
Mouse (Murine) Polyclonal GRIA1 Primary Antibody pour IHC (fro), IHC - ABIN152516
Kim, Kwon, Kim, Josselyn, Han: Memory recall and modifications by activating neurons with elevated CREB. dans Nature neuroscience 2013
These findings suggest that AKAP79, by orchestrating phosphorylation, represents a key to a GluA1 phosphorylation passcode, which allows the GluA1 subunit to escape GluA2 dominance and promote the appearance of CP-AMPARs.
These results indicate that GRIA1 rs2195450 C>T polymorphism is significantly associated with migraine risk.
Results found higher activating GluA1 phosphorylation at Serine 845 in brain samples from epileptic patients and provided evidence that GluA1 phosphorylation is modulated by GSK3B.
These findings indicate that the CaMKII-mediated GluA1 phosphorylation of S567 and S831 is critical for P2X2-mediated AMPAR internalization and ATP-driven synaptic depression.
The reversible binding of kynurenic acid (KYNA) on human glutamate receptor (GluR1) polypeptide (GluR1270-300)-modified gold surface has been studied at various temperatures under physiological conditions by two-dimensional SPR experiments. The registered sensorgrams were fitted by using different kinetic models without application of any commercial software. Results suggested that the binding reaction was exothermic.
Elevated GluA1 expression in spinal cord of the amyotrophic lateral sclerosis patients.
This study demonstrated that a significant decrease in the protein level of GluA1 in major depression disorder.
The findings do not support the association of GRIA1 SNPs with schizophrenia in the Chinese Han population.
Our data of this study confirmed the association of GRIA1 (rs2195450) to female migraine susceptibility in the Chinese Han population.
Polymorphisms in GRIA1 gene are a risk factor for asparaginase hypersensitivity during the treatment of childhood acute lymphoblastic leukemia
The level of phosphorylated GluA1 at S831 and S845, two major sites implicated in AMPAR regulation, is almost negligible. Results impel us to reconsider the mechanisms underlying synaptic plasticity.
This study failed to replicate previously reported association between GRIA1 rs548294 and migraine without aura, either as single marker or when analyzed in haplotype combination with rs2195450.
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.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor desensitization.
insight into the structure and function of the C-terminal domain of GluA1, which controls AMPA receptor function and trafficking during synaptic plasticity in the central nervous system.
Inhibition of CREB function is associated with a specific reduction of AMPA receptor subunit GluA1.
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.
human hippocampal samples from neonatal seizure autopsy cases also showed an increase in GluR1 S831 and S845.
These results suggest that GRIA1 polymorphism may have influence upon the risk of developing schizophrenia.
Glioblastoma brain tumor initiating cells express high concentrations of functional calcium-permeable AMPA receptors, raising the possibility that glutamate secretion in the GBM tumor microenvironment may stimulate brain tumor derived cancer stem cells.
The suppressing activity of mGlu1 receptors on mGlu5 receptor was maintained in mature PCs, suggesting that expression of mGlu1alpha and mGlu5 receptors is mutually exclusive in Purkinje cells. These findings add complexity to the the finely tuned mechanisms that regulate PC biology during development and in the adult life and lay the groundwork for an in-depth analysis of the role played by mGlu5 receptors in PC matur...
Metabotropic Acetylcholine and Glutamate Receptors Mediate PI(4,5)P2 Depletion and Oscillations in Hippocampal CA1 Pyramidal Neurons in situ.
The findings demonstrate that nucleus accumbens excitatory signaling via Gria1 expression is integral to the effects of Clock gene disruption on manic-like behaviors.
An abnormality in GluA1 palmitoylation led to hyperexcitability, resulting in epileptic seizure.
We analyzed the presence and clearance of TAM and its metabolites (N-desmethyl-tamoxifen, 4-hydroxytamoxifen and endoxifen) in brain and serum of mice by liquid chromatographic-high resolution-tandem mass spectrometry (LC-HR-MS/MS) and assessed optimal injection protocols by quantitative RT-PCR of several floxed target genes (p2ry1, gria1, gabbr1 and Rosa26-tdTomato locus).
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.
A striking reduction of EEG power density including the spindle-frequency range (10-15 Hz) during sleep in Gria1(-/-) mice. The reduction of spindle-activity in Gria1(-/-) mice was accompanied by longer REM sleep episodes, increased EEG slow-wave activity in the occipital derivation during baseline sleep, and a reduced rate of decline of EEG slow wave activity (0.5-4 Hz) during NREM sleep after sleep deprivation.
chronic alcohol consumption may promote the development of persistent postsurgical pain by enhancing AMPA receptor GluA1 Ser831 phosphorylation.
These results demonstrate that GluA1 plays a role in responding on the basis of palatability rather than other properties, such as the automatic and learnt post-ingestive, nutritional consequences of sucrose.
defects in the brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway contribute to the deregulated AMPAR trafficking.
The nucleus-accumbens-specific knockdown of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc.
Data indicate a key role of FoxO3a/Zdhhc3/GluA1 axis in the high-fat diet (HFD)-dependent impairment of cognitive function.
translocation of surface GluA1, but not GluA2, AMPAR subunits to the synapse requires the amino-terminal domain
Taken together, these results suggest that ApoE4 enhances Abeta inhibition of insulin-stimulated AMPA receptor function, which accelerates memory impairment in ApoE4xAPP mice.
Both hippocampal as well as extra-hippocampal GluA1-containing AMPA receptors contribute to spatial working memory.
Presynaptic (CA3 pyramidal cell), but not postsynaptic (CA1 pyramidal cell), deletion of N-methyl-d-aspartate (NMDA)-type glutamate receptors eliminated the ketamine-induced enhancement of excitatory synaptic transmission in hippocampal slices and the antidepressant actions of ketamine
In the present study, by combining a 64-channel multielectrode system and a novel analysis and visualization method, we observed the accurate spatial localization and dynamic temporal changes of network fEPSP signals and LTP responses within the ACC circuit and found that PKA phosphorylation, but not PKC phosphorylation, of the GluA1 is required for LTP in the ACC.
Data suggest that phosphorylation of Shp2/Ptpn11 at Tyr542 and its translocation to postsynaptic compartment are integral processes in synaptic scaling/homeostasis; Shp2 phosphatase activity is critical to regulation of Ser(P)845 GluA1 and surface expression of GluA1 during synaptic scaling. (Shp2/Ptpn11 = protein tyrosine phosphatase non-receptor type 11; GluA1 = glutamate receptor ionotropic Ampa1 [alpha 1])
Gria1 expression in Purkinje cells is not required for cerebellar motor learning.
Three epilepsy-associated missense mutations reduce neural precursor cell expressed developmentally down-regulated gene 4-2 (Nedd4-2)-mediated AMPA receptor GluA1 ubiquitination.
the intracellularly located CTD of GLUR1 is the origin of TARP-specific functional modulation and not merely a facilitator of trafficking
Low concentrations of quinine are decoded in interneuron AIB by low-threshold, fast-inactivation glutamate receptor GLR-1 and translated into reversal initiation. In contrast, high concentrations of quinine are decoded by high-threshold, slow-inactivation glutamate receptor GLR-5
We also assessed ionotropic glutamate receptor GLR-1 cell-specifically within AIB and determined that GLR-1 fine-tunes AIB activity to modify locomotion following reversal events. Our research highlights that signal integration underlying the initiation and fine-tuning of backwards locomotion is AIB and NPR-9 dependent, and has demonstrated the suitability of C. elegans for analysis of multisensory integration
We propose a model in which synaptic activity regulates the nuclear localization of CMK-1 to mediate a negative feedback mechanism coupling GLR-1 activity with its own transcription.
Mutants lacking p38 MAPK components pmk-1 or sek-1 resemble mutants lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate receptor GLR-1, and depression of GLR-1-mediated behaviors.
KEL-8 is a substrate receptor for Cullin 3 ubiquitin ligases that is required for the proteolysis of GLR-1 receptors and suggest a novel postmitotic role in neurons for Kelch/CUL3 ubiquitin ligases.
WDR-20 and WDR-48 form a complex with USP-46 and stimulate the DUB to deubiquitinate and stabilize GLR-1 in vivo.
glr-1 is required for long-term memory for habituation and memory for context conditioning.
Study indicates kinesin KLP-4 as a novel regulator of anterograde GLR-1 glutamate receptors trafficking and reveals a cellular control mechanism by which receptor cargo is targeted for degradation in tje absence of its motor.
An auxiliary protein SOL-2, a CUB-domain protein, associates with both the related auxiliary subunit SOL-1 and with the GLR-1 AMPA receptor.
UEV-1 could regulate a small subset of K63-linked ubiquitination events in nematodes, at least one of which is critical in regulating GLR-1 trafficking
results show that while the osmotic avoidance response requires both NMDA and non-NMDA receptors, the response to mechanical stimuli only requires non-NMDA receptors
Long-term memory in C. elegans is dependent on glr-1 and likely involves changes in the expression or localization of glutamate receptors
SOL-1 participates in the gating of non-NMDA (N-methyl-D-aspartate) iGluRs, thereby providing a previously unknown mechanism of regulation for this class of neurotransmitter receptor
GLR-1 is regulated in a homeostatic manner and this effect depends on clathrin-mediated endocytosis.
unfolded protein response signaling is a critical step in neural function that is needed for GLR-1, GLR-2, and GLR-5 assembly and secretion
Cytosolic tail sequences and subunit interactions of GLR-1 and GLR-2 are critical for synaptic localization of glutamate receptors
SOL-1 is an auxiliary subunit that modulates the gating of GLR-1 glutamate receptors
A critical period for the 3-day enhanced behavior and ionotropic glutamate receptor distribution was observed in first larval stage worms, whereas there was no critical period for the depressed effects observed in 5-day-old worms.
CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.
GLR-1-mediated avoidance behaviors are completely disrupted in stg-1;stg-2 double mutants, and GLR-1-mediated currents are absent, despite apparently normal surface expression of GLR-1.
The GRIA1 polymorphism exists in beef cows but it does not influence antral follicle numbers. The association between GnRHR genotype and age at first calving is likely not causal as this polymorphism is not functional.
Data show that GRIA1 is a critical mediator of ovulation and that GRIA1 might be a useful target for reproductive therapy.
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 with multiple subunits, each possessing transmembrane regions, and all arranged to form a ligand-gated ion channel. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. This gene belongs to a family of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, AMPA-selective glutamate receptor 1
, glutamate receptor 1
, glutamate receptor A
, glutamate receptor subunit GluR1
, glutamate receptor, ionotropic, AMPA1 (alpha 1)
, glutamate receptor ionotropic, AMPA 1
, AMPA glutamate receptor
, glutamate receptor, ionotropic, AMPA 1
, GluR1 protein
, glutamate receptor, ionotropic, AMPA 1.2
, glutamate receptor, ionotropic, AMPA 1b
, AMPA receptor subunit GluR1A
, glutamate receptor, ionotropic, AMPA1.1
, ionotropic glutamate receptor AMPA 1