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anti-Human GRIK1 Antibodies:
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Human Polyclonal GRIK1 Primary Antibody for IHC, ELISA - ABIN1002375
Tanaka: Functions of glutamate transporters in the brain. in Neuroscience research 2000
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Human Polyclonal GRIK1 Primary Antibody for IHC, ELISA - ABIN1002376
Pinheiro, Mulle: Kainate receptors. in Cell and tissue research 2006
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Human Polyclonal GRIK1 Primary Antibody for IHC (p), WB - ABIN541655
Bureau, Bischoff, Heinemann, Mulle: Kainate receptor-mediated responses in the CA1 field of wild-type and GluR6-deficient mice. in The Journal of neuroscience : the official journal of the Society for Neuroscience 1999
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Human Polyclonal GRIK1 Primary Antibody for IHC (p), WB - ABIN541654
Christensen, Paternain, Selak, Ahring, Lerma: A mosaic of functional kainate receptors in hippocampal interneurons. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2004
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Human Polyclonal GRIK1 Primary Antibody for ELISA, WB - ABIN261119
Martin, Nishimune, Mellor, Henley: SUMOylation regulates kainate-receptor-mediated synaptic transmission. in Nature 2007
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DRD2 A2/A1, DRD3 Ser9Gly, DbetaH -1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A are not associated with alcoholism alone or in interaction.
The findings reported here suggest that, in participants with the GRIK1 rs2832407*CC genotype, topiramate treatment enhances self-efficacy and reduces heavy drinking.
Findings indicate that SNPs in the GRIK1 gene is associated with altered cue-induced brain activation that is related to craving for alcohol and relapse risk.
Results suggested that the extracellular N-terminal region including the two CUB domains was largely responsible for the distinct regulatory effects of Neto1 and Neto2 on the desensitization properties of GluK1 homomeric receptors
In the present study, we have shown that gene-gene interaction of components of different systems associated with nicotine reinforcing effects, such as OPRM1 and GRIK1, rather than one gene polymorphism, is associated with smoking behavior.
This found that, among rs2832407*C of GRIK1 homozygotes, topiramate treatment produced the greatest reductions in the expected positive effects of drinking and desire to drink during the treatment period.
These results suggest that the effect of topiramate on drinking behavior, in which the GluK1-containing kainate receptor appears to play a key role, can be dissociated from its effect on weight.
Topiramate treatment for alcohol dependence was significantly more effective in rs2832407 C-allele homozygotes.
Reduced Homer binding to mGluR5 supports an inhibitory role for Homer interactions with mGluR5 in mediating neuropathy.
Using the SNaPshot assay, we present evidence for allelic nondisjunction at rs363506 in the GRIK1 gene and rs2834235 and rs7283354 in the GARS-AIRS-GART gene in Down syndrome in India.
The association at rs455804 implicates GRIK1 as a novel susceptibility gene for HBV-related HCC, suggesting the involvement of glutamate signaling in the development of HBV-related HCC.
GRIK1 rs469472 to be possibly associated with schizophrenia in our independent case-control and family samples
Presynaptic Gluk1 kainate receptors that reduce transmitter release downstream are independent of divalent calcium ion Ca2+ influx.
The amino acid sequence of the GluK1 kainate receptor near or within the carboxyl-terminal endoplasmic reticulum retention signal sequence, which affects receptor trafficking and/or expression, does not affect channel gating properties.
The GRIK1 promoter is activated by Trichostatin A (TSA) treatment and by serum depletion according to promoter reporter assays in HEK 293 cells.
findings show GluR5 was upregulated in the hippocampus, but not in the temporal neocortex, of patients with temporal lobe epilepsy (TLE)compared to controls; mossy fiber sprouting in the hippocampus of TLE patients was correlated with GluR5 upregulation
Variation in the 3' portion of the gene encoding the GluR5 kainate receptor subunit contributes to the risk for alcohol dependence.
GluK1 kainate receptor polymorphisms are associated with Down syndrome.
GRIK1 does not play a major role in schizophrenia pathogenesis in the Japanese population
there are trafficking signals in the C-terminal domain of GluR5-2b; alternative splicing is an important mechanism regulating KAR function
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...
These effects correlate with the mGluR5 over-expression.
loss of FMRP leads to the abnormal function and localization of kainite receptors.
Data (including data from in vitro studies using tissues from transgenic mice) suggest that vitamin D3 suppresses NMDA-receptor- (Grin1)-mediated and kainate-receptor- (Grik1)-mediated excitation of GnRH- (gonadotrophin-releasing hormone)-secreting neurons of pre-optic area of hypothalamus. These studies were conducted with brain slices from male and female mice in pre-pubertal period.
The cytoplasmic domain of the GluK2 low-affinity subunit stabilizes kainate receptors at synapses. In contrast, the extracellular domain of the GluK4/5 high-affinity subunit synergistically controls the synaptic specificity of kainate receptors through interaction with C1q-like proteins.
GluK5 is almost exclusively localized to the presynaptic ribbon of photoreceptor terminals.
These data reveal some requirements for kainate receptor targeting to the synapse, indicating a fundamental role of high affinity kainate receptor subunits in this process.
These results establish critical roles for Neto auxiliary subunits controlling Kainate receptor properties and synaptic incorporation.
Animals trained in the trace fear conditioning protocol exhibited a transient increase in unedited GRIK1 RNA in the amygdala, and their learning efficiency correlated with unedited RNA levels in CA1.
results show that GluK1 and Go proteins are natural partners, accounting for the metabotropic effects of Kainate receptors.
integrity of Homer scaffolds is essential for normal glur5-evoked endocannabinoid functioning
We combine pharmacological, genetic, and electrophysiological approaches to show that cortical GluK1-containing kainate (KA) receptors are involved in scratching induced by histamine and non-histamine-dependent itching stimuli
The combined loss of the AMPA receptor auxiliary TARPg-2 subunit and the GluK5 subunit leads to early mouse lethality.
CaMKII-dependent phosphorylation of GluK5 is responsible for synaptic depression by untrapping of KARs from the PSD and increased diffusion away from synaptic sites.
these data further implicate Group 1 mGluR signaling through Homer2 within the nucleus accumbens in excessive alcohol consumption
This study demonistrated that grik1 gene expression in mouse dorsal raphe nucleus
Activation of presynaptic GluK1 kainate receptors at lateral amygdala synapses results in the inhibition of glutamate release and the coupling of GluK1 receptors to a cascade involving the regulation of protein kinase A (PKA) activity.
This study demonistrated that glutamate signaling through mGluR5 located on dopamine D1 receptor-expressing neurons is necessary for incentive learning processes that contribute to cue-induced reinstatement of cocaine-seeking.
These results show that the GluR5 subunits are expressed functionally on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice
these results establish an integral role for mGluR5 and ERK1/2 in nociceptive processing in the amygdala.
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 the kainate family of glutamate receptors, which are composed of four subunits and function as ligand-activated ion channels. The subunit encoded by this gene is subject to RNA editing (CAG->CGG\; Q->R) within the second transmembrane domain, which is thought to alter the properties of ion flow. Alternative splicing, resulting in transcript variants encoding different isoforms, has been noted for this gene.
glutamate receptor, ionotropic, kainate 1
, glutamate receptor, ionotropic kainate 1
, excitatory amino acid receptor 3
, glutamate receptor 5
, glutamate receptor ionotropic, kainate 1
, glutamate receptor subunit 5