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anti-Human GRIN1 Antikörper:
anti-Rat (Rattus) GRIN1 Antikörper:
anti-Mouse (Murine) GRIN1 Antikörper:
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Mammalian Monoclonal GRIN1 Primary Antibody für ISt, IHC - ABIN1304678
Maraschi, Ciammola, Folci, Sassone, Ronzitti, Cappelletti, Silani, Sato, Hattori, Mazzanti, Chieregatti, Mulle, Passafaro, Sassone: Parkin regulates kainate receptors by interacting with the GluK2 subunit. in Nature communications 2014
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Human Monoclonal GRIN1 Primary Antibody für ICC, IF - ABIN152467
Nagy, Kolok, Dezso, Boros, Szombathelyi: Differential alterations in the expression of NMDA receptor subunits following chronic ethanol treatment in primary cultures of rat cortical and hippocampal neurones. in Neurochemistry international 2002
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Human Monoclonal GRIN1 Primary Antibody für BI, IHC - ABIN967491
Brose, Huntley, Stern-Bach, Sharma, Morrison, Heinemann: Differential assembly of coexpressed glutamate receptor subunits in neurons of rat cerebral cortex. in The Journal of biological chemistry 1994
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Rat (Rattus) Polyclonal GRIN1 Primary Antibody für ICC, IF - ABIN251579
González-González, Henley: Postsynaptic kainate receptor recycling and surface expression are regulated by metabotropic autoreceptor signalling. in Traffic (Copenhagen, Denmark) 2013
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Human Polyclonal GRIN1 Primary Antibody für IHC (p), WB - ABIN3044347
Shang, Luo, Deng, Wang, Huang, Feng, Yue: Expression of N-methyl-D-aspartate receptor and its effect on nitric oxide production of rat alveolar macrophages. in Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society 2010
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Data suggest GRINL1A (GCOM1 (zeige GRINL1A Antikörper))-NMDA receptor-internexin-alpha (INA (zeige INA Antikörper)) interaction pathway may be relevant to neuroprotection.
These results indicate these individuals may have suffered neurodevelopmental deficits as a result of the decreased presence of GluN1-G620R/GluN2B (zeige GRIN2B Antikörper) complexes on the neuronal surface during embryonic brain development and reduced current responses of GluN1-G620R-containing NMDARs after birth.
Mice with GRIN1 disrupted in the intralaminar thalamic nuclei exhibited various schizophrenia-like phenotypes, including deficits in working memory, long-term spatial memory, and attention, as well as impulsivity, impaired prepulse inhibition, hyperlocomotion and hyperarousal.
2-methoxyestradiol impacts on glycine/serine-mediated metabolic reprogramming in osteosarcoma cells by its interaction with GRIN1/GluN2A (zeige GRIN2A Antikörper) receptors.
tPA (zeige PLAT Antikörper) is a ligand of the N-terminal domain of the obligatory GluN1 subunit of NMDAR acting as a modulator of their dynamic distribution at the neuronal surface and subsequent signaling.
Two novel Grin1 mutations were identified in 2 cases of severe early infantile encephalopathy. Se688Tyr mutation results in disruption of NMDA ligand binding and the p.Gly827Arg mutation results in disrupted gating of the ion channel.
A homozygous missense variant of GRIN1 was identified in two consanguineous sibs affected with severe intellectual disability and autistic features.
NMDA receptor-dependent signaling is involved in melanosome transfer, which is associated with calcium influx, cytoskeleton protein (zeige SPTBN1 Antikörper) redistribution, dendrites and filopodia formation
Findings show that N-methyl-d-aspartic acid receptor subunit GluN1 is expressed on oligodendrocytes and myelin in humans.
De novo GRIN1 mutations are associated with severe intellectual disability with cortical visual impairment as well as oculomotor and movement disorders being discriminating phenotypic features. Loss of NMDA receptor function appears to be the underlying disease mechanism. The identification of both heterozygous and homozygous mutations blurs the borders of dominant and recessive inheritance of GRIN1-associated disorders.
Establishment of late-phase long-term potentiation (L-LTP (zeige SCP2 Antikörper)) in vivo requires NMDAR activation in the postsynaptic tectal cells within a critical time window after LTP (zeige SCP2 Antikörper) induction.
PIP2 supports the open state of NMDA receptors via the adaptor protein alpha-actinin (zeige ACTN1 Antikörper). PIP2 and alpha-actinin (zeige ACTN1 Antikörper) act like a two-component hinge keeping the channel gate in its open state.
We demonstrate that neocortical neurons that have only one copy of Sip1 (zeige ZEB2 Antikörper) (heterozygous, Sip1 (zeige ZEB2 Antikörper)(fI/wt)), are more sensitive to both NMDA- and AMPA (zeige GRIA3 Antikörper)- receptors agonists as compared to wild type neurons (Sip1 (zeige ZEB2 Antikörper)(wt/wt)).
Study shows that social isolation to a series of schizophrenia-related deficits and that potential interactions among histidine triad nucleotide binding protein 1 (zeige HINT1 Antikörper), NMDA receptor 1, and dopamine receptor 2 (zeige DRD2 Antikörper) may underlie the behavioral deficits induced by social isolation.
We found that the inducible deletion of the NMDA receptors prior to behavioral assays impaired, not only object and social recognition memory tests, but also resulted in profound deficits in social motivation. Mice with ablated NR1 subunits in the forebrain demonstrated significant decreases in sociability compared to their wild type counterparts.
Isoflurane relieves zymosan-induced neutrophil inflammatory lung response by targeting NMDA glutamate receptor and Toll-like receptor 2 signaling pathway.
Sepsis selectively decreased the protein and mRNA levels of GluN2A (zeige GRIN2A Antikörper), GluN2B (zeige GRIN2B Antikörper) and GluN1 but not the levels of synaptophysin (zeige SYP Antikörper) or the neuronal number in the hippocampus of septic mice.
The present study provides additional support for roles for GRIN1 in the etiology of depression following early adversity.
NMDARs are critical for developmental programs involved in appropriate expression of short-term plasticity, AMPA (zeige GRIA3 Antikörper) receptor (AMPAR) function and dendrite patterning.
Study showed that NR1(D1CreERT2) mice lack the ability to associate contextual cues with the rewarding effects of drugs of abuse, with minor or no deficits in other reward-conditioned behaviors or learning in general.
tau overexpression mediates the excitatory toxicity induced by E-NMDAR activation through inhibiting ERK (zeige EPHB2 Antikörper) phosphorylation.
GluN1 deletions in D1- and A2A-expressing cell types reveal distinct modes of behavioral regulation. The data supports the hypothesis that cell type-specific NMDAR signaling regulates separable behavioral outcomes related to locomotion, despair, and relapse.
The protein encoded by this gene is a critical subunit of N-methyl-D-aspartate receptors, members of the glutamate receptor channel superfamily which are heteromeric protein complexes with multiple subunits arranged to form a ligand-gated ion channel. These subunits play a key role in the plasticity of synapses, which is believed to underlie memory and learning. Cell-specific factors are thought to control expression of different isoforms, possibly contributing to the functional diversity of the subunits. Alternatively spliced transcript variants have been described.
N-methyl-D-aspartate receptor channel, subunit zeta-1
, N-methyl-D-aspartate receptor subunit NR1
, glutamate [NMDA] receptor subunit zeta 1
, glutamate [NMDA] receptor subunit zeta-1
, glutamate receptor ionotropic, NMDA 1
, N-methyl-D-aspartate receptor
, NMDA glutamate receptor
, glutamate receptor, ionotropic, N-methyl D-aspartate 1
, N-methyl-D-aspartate glutamate receptor
, NMDA R1 receptor C1 cassette
, neurotransmitter receptor
, NMDA-type glutamate receptor 1
, NMDA-type glutamate receptor subunit 1
, N-methyl-D-aspartate receptor 1
, Glutamate [NMDA] receptor subunit zeta-1
, glutamate receptor subunit zeta 1
, N-methyl-D-aspartate receptor type 1