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Results suggest a role for GluA3 channel activity in the regulation of sleep behavior in both mice and humans.
GluA3 is required for normal auditory signaling, normal ultrastructure of AN-BC synapses in the cochlear nucleus and normal experience-dependent changes in auditory processing after transient sound reduction.
These experiments indicate that the presence of GluA3-containing AMPARs is critical for Abeta (zeige APP Antikörper)-mediated synaptic and cognitive deficits.
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP (zeige SCP2 Antikörper)), but not long term depression, at parallel fiber-Purkinje cell synapses. GluA3-dependent potentiation involves a cAMP-driven change in channel conductance. GluA3-mediated LTP (zeige SCP2 Antikörper) and learning are induced via cAMP-mediated Epac (zeige RAPGEF3 Antikörper) activation.
These results provide direct evidence for cortical AMPA receptors to contribute to zymosan-induced visceral and spontaneous pain.
Data indicate that the AMPA receptor subunits abundance is hippocampus, GluA2 (zeige GRIA2 Antikörper) > GluA1 (zeige GRIA1 Antikörper) > GluA3 >> GluA4 (zeige GRIA4 Antikörper); cortex, GluA2 (zeige GRIA2 Antikörper) > GluA3 >/= GluA1 (zeige GRIA1 Antikörper) >> GluA4 (zeige GRIA4 Antikörper); and cerebellum, GluA2 (zeige GRIA2 Antikörper) > GluA3 >/= GluA1 (zeige GRIA1 Antikörper) > GluA4 (zeige GRIA4 Antikörper).
This study demonistrated that Gria3 gene expression in mouse dorsal raphe nucleus
This study demonistrated that the GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum.
GluR2 (zeige GRIA2 Antikörper) and GluR3 subunits of AMPA receptor play roles in the trigeminal nerve injury-mediated enhancement of neuronal excitability and hyperalgesia.
Mice treated with anti-Glur3 antisense peptide nucleic acids had significantly extended survival compared to mice injected with a nonsense sequence in a mouse model of Amyotrophic lateral sclerosis
Our findings support the GWAS-implicated link between GRM3 (zeige GRM3 Antikörper) 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 (zeige SLC9A3R1 Antikörper) and NHERF-2 (zeige SLC9A3R2 Antikörper) (Na+/H+ exchanger regulatory factors 1 and 2) in regulating the distribution of Group II metabotropic glutamate (zeige GRIN1 Antikörper) receptor (mGluRs) in the murine brain, while conversely the effects of the mGluR2 (zeige GRM2 Antikörper)/3 PDZ (zeige INADL Antikörper)-binding motifs on receptor signaling are likely mediated by interactions with other PDZ (zeige INADL Antikörper) scaffold proteins beyond the NHERF (zeige SLC9A3R1 Antikörper) proteins.
Results demonstrate that GRM3 (zeige GRM3 Antikörper) expression is significantly upregulated in human colonic adenocarcinomas and colon cancer cell lines. This upregulation is mediated at the post-transcriptional level where miR (zeige MLXIP Antikörper)-487b directly targets GRM3 (zeige GRM3 Antikörper) to suppress its translation. Also, the fact that TGFbeta (zeige TGFB1 Antikörper) increases GRM3 (zeige GRM3 Antikörper) protein stability provide novel mechanisms of post-transcriptional regulation of GRM3 (zeige GRM3 Antikörper) in colon cancer.
Low GRM3 (zeige GRM3 Antikörper) 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 (zeige GRM3 Antikörper) rs274622 C carriers with schizophrenia were associated with significantly smaller prefrontal activation than patients with TT genotype
Grm3 (zeige GRM3 Antikörper) 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 (zeige GRM3 Antikörper) variants and symptom response to antipsychotics.
PI4KA (zeige PI4KA Antikörper) and GRM3 (zeige GRM3 Antikörper) polymorphisms have potential to jointly modulate antipsychotic response
Findings suggest that mGluR2 (zeige GRM2 Antikörper)/3 and mGluR5s are unaltered in the anterior cingulate cortex in psychotic and nonpsychotic depression, bipolar disorder and schizophrenia
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.
AMPA-selective glutamate receptor 3
, glutamate receptor 3
, glutamate receptor, ionotrophic, AMPA 3
, glutamate receptor, ionotropic, AMPA3 (alpha 3)
, glutamate receptor channel alpha3 subunit
, glutamate receptor subunit 3
, glutamate metabotropic receptor 3
, metabotropic glutamate receptor 3