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anti-Human GRM2 Antibodies:
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Cow (Bovine) Polyclonal GRM2 Primary Antibody for IHC (fro), WB - ABIN550157
Wilson, Nicoll: Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses. in Nature 2001
Show all 3 Pubmed References
Human Polyclonal GRM2 Primary Antibody for ELISA, IHC - ABIN4334107
So, Fong, Chen, Hui, Ng, Cherny, Mak, Cheung, Chan, Chen, Li, Sham: Identification of neuroglycan C and interacting partners as potential susceptibility genes for schizophrenia in a Southern Chinese population. in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 2009
data suggests that glutamatergic activity through GRM2 in cerebral cortex may differ with gender and suicide ideation.
mGlu2 receptors can play an influential role in reducing the probability of glutamate neurotransmitter release and potentially effect seizure activity.
Studies support a role for NHERF-1 and NHERF-2 (Na+/H+ exchanger regulatory factors 1 and 2) in regulating the distribution of Group II metabotropic glutamate receptor (mGluRs) in the murine brain, while conversely the effects of the mGluR2/3 PDZ-binding motifs on receptor signaling are likely mediated by interactions with other PDZ scaffold proteins beyond the NHERF proteins.
The present data demonstrateD that a mechanism of group II mGluR-induced analgesia identified in rodent sensory neurons translates mechanistically to human sensory neurons
this work offers new insights into the functioning of the mGlu2 receptor, which might contribute to the development of new and improved PAMs
Allosteric signaling through an mGlu2 and 5-HT2A heteromeric receptor complex and its potential contribution to schizophrenia.
Study furthers our understanding of positive allosteric modulation of the mGlu2 receptor and can contribute to improved future design of mGlu2 modulators.
Findings suggest that mGluR2/3 and mGluR5s are unaltered in the anterior cingulate cortex in psychotic and nonpsychotic depression, bipolar disorder and schizophrenia
Results demonstrate no changes in expression and density of both 5-HT2AR and mGlu2/3R in the postmortem prefrontal cortex of subjects with major depressive disorder under basal conditions; antidepressant treatment induces a decrease in 5-HT2AR density
Human anterior cingulate cortex from alcoholic patients shows a significant reduction in mGluR(2) transcripts compared to control subjects
Three residues located at the intracellular end of transmembrane domain four are necessary for the mGlu2 receptor binding to 5TR2A.
the promoter methylation of the GMR2 and GMR5 genes greatly decreased the risk of schizophrenia, and the expression level of the GRM2, GRM5, and GRIA3 genes increased significantly in patients in comparison to healthy controls.
the structural properties for the H8 domain of the mGluR2 receptor; H8 behaves as a sensor of cholesterol concentration.
Only full-length dimeric mGlu2 activates G protein upon glutamate binding.
Suggest a genetic association exists between SNPs in several genes, such as HTR2A and NRG1, and response to mGlu2/3 agonist LY2140023 treatment in schizophrenia.
data support the idea that glutamate release in the vental tegmental area(VTA) is critically involved in cocaine-induced reinstatement; loss of mGluR2/3-mediated regulation of glutamate release in the VTA may critically contribute to the risk of relapse
Our results suggested that GRM2 may play a role in the pathophysiology of methamphetamine-induced psychosis but not schizophrenia in the Japanese population
This study demonistrated that the level of metabotropic glutamate receptor 2/3 is elevated in the prefrontal cortex in patient of major depression disorder.
No association is detected between GRM2 and major depressive disorder or bipolar disorder in an allele/genotype-wise or haplotype-wise analysis of Japanese patients.
Mapped to Chromosome 3p21.1 - p21.2 and has 5 exons ranging from 74 - 1076 bp.
Here we show that glutamate signals through metabotropic glutamate receptor 2 (mGluR2) to induce Erk phosphorylation in SC. mGluR2-elicited Erk phosphorylation requires ErbB2/3 receptor tyrosine kinase phosphorylation to limit the signaling cascade that promotes phosphorylation of Erk, but not Akt.
activation of mGlu2 receptors is detrimental in the post-ischemic phase, and support the use of mGlu2 receptor antagonists in the experimental treatment of brain ischemia.
mGlu2 activation exerts effects on striatal physiology that extend beyond modulation of corticostriatal synapses, and has the potential to influence cognition and striatum-related disorders via inhibition of thalamus-derived glutamate and dopamine release.
These studies provide a foundation for future research seeking to parse out the roles of mGlu2 from mGlu3, paving the way for better understanding of how these receptors regulate activity in the brain.
provided evidence that JARID1B via modulation of stemness-related signaling is a putative novel therapeutic target for treating malignant NB
Activation of GABA(B) or mGlu2/3 receptors inhibited both evoked presynaptic Ca(2+) transients and striatal field potentials.
In GRM2 knockout mice motor coordination and cognition is unchanged compared to GRM2/3 double knockout mice.
activation of both Group I and Group II metabotropic glutamatergic receptors suppress retinogeniculate transmission
The findings support the possibility that interactions between mGlu2/3 and dopamine may be relevant to the pathophysiology and therapy of schizophrenia and other disorders
mGluR3 knockouts did not differ from controls in reinstatement of drug-seeking behavior, suggesting that mGluR2 receptors are critical in mediating addictive-like behavior.
In the central nervous system, mGluR2 and mGluR4 form a hetero-complex with a distinct pharmacological profile.
The reduction in the expression of mGluR2 and mGluR3 may be involved in the development of benzodiazepine dependence.
5-HT(2A) receptor-dependent signaling epigenetically affects mGlu2 transcription in mouse frontal cortex.
The mGluR2 subtype activates an inwardly rectifying potassium conductance in dendrites of the dentate gyrus.
L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors.
Restraint stress induces a schizophrenia-like phenotype in mice, with epigenetic changes in mGlu2 and mGlu3 receptors that lie at the core of pathological programming induced by early-life stress.
Fractionation of hippocampus-dependent memory depending on the appetitive-aversive context is to our knowledge unique, and suggests a role for group II metabotropic GluRs at the interface of arousal and cognition.
Isolation rearing causes an increase in mGluR2 receptors in prefrontal cortex and hippocampus.
L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors, that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties. Group I includes GRM1 and GRM5 and these receptors have been shown to activate phospholipase C. Group II includes GRM2 and GRM3 while Group III includes GRM4, GRM6, GRM7 and GRM8. Group II and III receptors are linked to the inhibition of the cyclic AMP cascade but differ in their agonist selectivities. Two transcript variants encoding different isoforms have been found for this gene.
glutamate metabotropic receptor 2
, glutamate receptor homolog
, metabotropic glutamate receptor 2
, G protein coupled receptor, family C, group 1, member B
, G protein-coupled receptor, family C, group 1, member B