No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human Metabotropic Glutamate Receptor 3 Antibodies:
anti-Mouse (Murine) Metabotropic Glutamate Receptor 3 Antibodies:
anti-Rat (Rattus) Metabotropic Glutamate Receptor 3 Antibodies:
Go to our pre-filtered search.
Human Polyclonal Metabotropic Glutamate Receptor 3 Primary Antibody for ELISA - ABIN545364
Shiraishi, Misumi, Takama, Takahashi, Shoji: Myristoylation of human immunodeficiency virus type 1 gag protein is required for efficient env protein transportation to the surface of cells. in Biochemical and biophysical research communications 2001
Show all 3 Pubmed References
this study demonstrates that metastasized cells are less migratory due in part to the post-metastatic downregulation of S100A4 and GRM3. Targeting S100A4 and GRM3 may help prevent bone metastasis.
strong interaction between glutamate and Cl(-) ions allows the mGlu3 receptor to sense and efficiently react to sub-micromolar concentrations of glutamate, making it the most sensitive member of mGluR family
Tumor-associated GRM3 variants disrupted trafficking of melanosomes, causing their aggregation in the cell body in a cAMP-dependent manner.
experiments indicate that mGlu3Delta4 may negatively modulate mGlu3, and thereby impact on the roles of GRM3/mGlu3 in schizophrenia and as a therapeutic target
Our findings support the GWAS-implicated link between GRM3 genetic variation and schizophrenia risk as well as the notion that alleles conferring this risk may be population specific.
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.
Results demonstrate that GRM3 expression is significantly upregulated in human colonic adenocarcinomas and colon cancer cell lines. This upregulation is mediated at the post-transcriptional level where miR-487b directly targets GRM3 to suppress its translation. Also, the fact that TGFbeta increases GRM3 protein stability provide novel mechanisms of post-transcriptional regulation of GRM3 in colon cancer.
Low GRM3 expression is associated with multiple myeloma and B-cell leukemia.
Significant association was found between rs12704290 in GRM3 gene and schizophrenia(SCZ). A three-SNP LD spanning GRM3Delta4 splice site was significantly associated with SCZ. Interaction between the LD block and cognitive function was found in SCZ patients.
Results show that GRM3 rs274622 C carriers with schizophrenia were associated with significantly smaller prefrontal activation than patients with TT genotype
Grm3 expression was decreased in B cells from patients with autoimmune diseases such as activated systemic lupus erythematosus and multiple sclerosis.
Pharmacogenetic relationships were identified in patients with schizophrenia between GRM3 variants and symptom response to antipsychotics.
PI4KA and GRM3 polymorphisms have potential to jointly modulate antipsychotic response
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
The mGluR3 promoted the proliferation of human embryonic cortical NPCs and increased cyclin D1 expression by activating ERK1/2 and JNK2 signaling pathways.
The data of this study suggest an association of the GRM3 rs6465084 polymorphism with changes in pursuit maintenance after antipsychotic treatment.
This study provided that the evidence for an association between GRM3 genotype and schizophrenia and suggest a role for glutamate neurotransmission in the establishment and maintenance of myelinated fibers.
results supplied the first evidence that the polymorphism of GRM3 gene associates with the morbidity of alcohol dependence in human beings.
report we describe a novel neuroprotective function of mGlu3 receptors related to their ability to promote the non-amyloidogenic pathway of APP cleavage in astrocytes, thus enhancing sAPPalpha production
Loss of Nogo-A, encoded by the schizophrenia risk gene Rtn4, reduces mGlu3 expression and causes hyperexcitability in hippocampal CA3 circuits
the activation of mGluR3 up-regulates the membrane expression of TWIK-1 that in turn enhances NH4(+) uptake in astrocytes.
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.
Activation of Grm3 ameliorates lupus-like disease in mice by reducing B cell numbers. Grm3 expression on B-cells is decreased in lupus-prone mice.
The number of mGluR3-immunoractive cells was significantly reduced in the dorsal and intermediate but not ventral parts of the lateral septum in postpartum versus virgin females.
GRM3-knockout mice exhibit a biphasic effect in spatial working memory, initially impaired but performing better after training.
The results of these studies implicate mGlu3 as a major regulator of PFC function and cognition.
This study demonistrated that mGluR3 knockout mice show a working memory defect.
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.
The reduction in the expression of mGluR2 and mGluR3 may be involved in the development of benzodiazepine dependence.
study found that astrocytic expression of mGluR5 is developmentally regulated and is undetectable after postnatal week 3; mGluR3, whose activation inhibits adenylate cyclase but not calcium signaling, was expressed in astrocytes at all developmental stages
Restraint stress induces a schizophrenia-like phenotype in mice, with epigenetic changes in mGlu2 and mGlu3 receptors that lie at the core of the 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 (mGlu2/3)at the interface of arousal and cognition.
This study demonistrated that mGluR3 and not mGluR2 receptors mediate the efficacy of NAAG peptidase inhibitor in validated model of schizophrenia.
Following isolation rearing there is an increase in mGluR3 density in prefrontal cortex and hippocampus.
Hippocampal mossy fiber long-term depression in Grm2/3 double knockout mice.
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.
metabotropic glutamate receptor 3
, glutamate metabotropic receptor 3
, G protein-coupled receptor, family C, group 1, member C