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Both the GRIK2 rs4840200-T and rs3213607-A, and the interactions between rs4840200 and rs9390754 are related to the increased risk of epilepsy risk.
These results indicate involvement of GRIK2 in senescence and suggests GRIK2 as a potential target for therapeutic intervention of cancer cells.
Study identifies differentially variable CpG sites in GRIK2 gene displaying increased expression in patients with chronic obstructive pulmonary disease.
results suggest that PKC SUMOylation is an important regulator of the 14-3-3 and GluK2a protein complex and may contribute to regulate the decay kinetics of kainate receptor-excitatory postsynaptic currents
these findings indicate that GRIK2 has a role in the maintenance of urothelial cancer stem cells and that GRIK2 and ALDH1 can be prognosis prediction markers for urinary tract carcinomas
TTBK2 down-regulates GluK2 activity by decreasing the receptor protein abundance in the cell membrane via RAB5-dependent endocytosis.
In the Han population in Central China, the polymorphisms of SNP rs9390754 in the GRIK2 gene may be associated with epilepsy susceptibility.
Study demonstrates that co-assembly of recombinant kainate receptors (GluK1 and GluK2) with the Neto1 and Neto2 auxiliary subunits alters their onset and recovery from desensitization in a subunit-dependent manner
This study found in GRIK2 (glutamate receptor, ionotropic kainate 2) was most significant and also showed significant correlations with gene expression.
This study showed that Gluk2 association with obsessive-compulsive disorder.
Parkin interacts with the kainate receptor GluK2 subunit and regulates KAR function.
High risk genetic markers of paranoid schizophrenia were GRIK2*ATG and GRIK2*TGG in Tatars.
The present study reveals an additional mechanism for the regulation of GluK2-containing kainate receptors by Src family kinases, which may be of pathological significance in ischemic stroke.
we found no association between rs1556995 in GRIK2 and clozapine-induced obsessive-compulsive (OC) symptoms, implying that that GRIK2 may not play a role in the development of OC symptoms in schizophrenia patients
Crosslinking the ligand-binding domain dimer interface locks kainate receptors out of the main open state.
14-3-3 proteins are an important regulator of GluK2a-containing KARs and may contribute to the slow decay kinetics of native KAR-EPSCs.
Kainate receptor GluK2a post-translational modifications differentially regulate association with 4.1N to control activity-dependent receptor endocytosis
Eight chromosome 6 SNPs, having the most significant differences, were delineated: rs10499298, rs10499299, rs17827966, rs1224329, rs1150790, rs713050, rs2518344 and rs487083; all were associated with genes GRIK2.
The ACAG haplotype in the 13th haplotype block of the GRIK2 gene was associated with somatic anxiety.
Comprehensive analytical methods applied to a much larger sample than in previous studies do not support a role for GRIK2 as a genetic modifier of age at onset of clinical symptoms in Huntington's disease.
Hippocampal CA3 kainate receptors have been found to contribute to seizure activities.
loss of FMRP leads to the abnormal function and localization of kainite receptors.
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.
GluK2-mediated increase in KCC2 recycling to the surface membrane translates to a hyperpolarization of the reversal potential for GABA (EGABA).
Loss of parkin function in primary cultured neurons causes GluK2 protein to accumulate in the plasma membrane.
Interictal and ictal discharges are minimized in mice lacking the GluK2 subunit.
This study demonistrated that grik2 gene expression in mouse dorsal raphe nucleus
The results show that NETO2 is a kainate receptor subunit with significant effects on glutamate signaling mechanisms in brain.
GluR6 kainate receptors are critically involved in inhibiting transmission at both A delta and C fibre monosynaptic pathways. Presynaptic GluR5 kainate receptors play limited role in inhibiting C fibre-activated pathway.
role for kainate receptors in the maturation of mossy fibre synapses.
Using kainate receptor knock-out mice, we show that subunits glutamate receptor (GluR) 5 and GluR6 play distinct roles in kainate-induced gamma oscillations and epileptiform burst activity.
The facilitatory effects of kainate on mossy fiber synaptic transmission and plasticity are mediated by GLU(K6)-containing kainate receptors.
In the present study, we used knock-out mice to explore the contribution of GluR5 and GluR6 receptors to sensory responses, fear memory, and learning-related synaptic potentiation in the amygdala.
The related kinases SGK2 and SGK3 similarly stimulate GluR6, but are less effective than SGK1.
Thus, GluR6a and GluR6b bring in close proximity two separate subsets of interacting proteins that contribute to the fine regulation of KAR trafficking and function.
Gbeta5-RGS complexes co-localize with mGluR6 in retinal ON-bipolar cells.
The involvement of the kainate receptor subunit GluR6 (GRIK2) in mediating behavioral displays related to behavioral symptoms of mania
Our results are indicative of either down-regulation of kainate receptors or modulation of their functional characteristics in weaver (Girk2-wv mutant) granule cells.
To our knowledge, the present work is the first report of a GluK receptor as the target of chronic treatment with mood-stabilizing drugs. This effect was both drug-specific and receptor subtype-specific.
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 at multiple sites within the first and second transmembrane domains, which is thought to alter the structure and function of the receptor complex. Alternatively spliced transcript variants encoding different isoforms have also been described for this gene. Mutations in this gene have been associated with autosomal recessive mental retardation.
glutamate receptor 6
, glutamate receptor, ionotropic kainate 2
, glutamate receptor, ionotropic, kainate 5
, excitatory amino acid receptor 4
, glutamate receptor form A
, glutamate receptor form B
, glutamate receptor form C
, glutamate receptor form D
, glutamate receptor form E
, glutamate receptor ionotropic, kainate 2
, gluR beta-2
, glutamate receptor beta-2
, glutamate receptor, ionotropic, kainate 2