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anti-Human Metabotropic Glutamate Receptor 5 Anticorps:
anti-Rat (Rattus) Metabotropic Glutamate Receptor 5 Anticorps:
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Human Polyclonal Metabotropic Glutamate Receptor 5 Primary Antibody pour ELISA - ABIN542969
Pacheco, Ciruela, Casadó, Mallol, Gallart, Lluis, Franco: Group I metabotropic glutamate receptors mediate a dual role of glutamate in T cell activation. dans The Journal of biological chemistry 2004
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Mouse (Murine) Polyclonal Metabotropic Glutamate Receptor 5 Primary Antibody pour IHC (fro), IHC - ABIN152473
Spanagel, Pendyala, Abarca, Zghoul, Sanchis-Segura, Magnone, Lascorz, Depner, Holzberg, Soyka, Schreiber, Matsuda, Lathrop, Schumann, Albrecht: The clock gene Per2 influences the glutamatergic system and modulates alcohol consumption. dans Nature medicine 2005
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Study shows that anti-mGluR5 encephalitis associates with a complex neuropsychiatric syndrome, not restricted to limbic encephalitis, and can occur without tumor.
using a combination of X-ray crystallography, cryo-electron microscopy and signalling studies, presentation of a structural framework for the activation mechanism of metabotropic glutamate receptor subtype 5
Results suggests contribution of common variants of GRM5 to impaired attention and reduced right hippocampal volume in schizophrenia, particularly in men, suggesting these variants may operate in a sex-specific manner. The effect of rs3814927 on IQ may have further implications of these findings in other disorders in which GRM5 is also associated.
mGluR5 signaling in T cells may play a key role in the development of chronic inflammation resulting in fatigue and contribute to individual differences in immune responses to radiation.
clinical evidence for altered mGluR5 signaling in the amygdala in alcohol use disorder
We anticipate that the resulted outcome could be supportive to discover potent negative allosteric modulators for metabotropic glutamate receptor 5 (mGluR5).
This study provides information concerning the changes in the expression of GABAergic and glutamatergic markers in mice lacking the mGlu5.
We report that expression of a key regulator of synaptic protein synthesis, the metabotropic glutamate receptor 5 (mGlu5) protein, is significantly reduced in both the brains of RS model mice and in the motor cortex of human RS autopsy samples.
once at the inner nuclear membrane, mGluR5 is stably retained via interactions with chromatin and is perfectly positioned to regulate nucleoplasmic Ca(2+)in situ
Overall, these data posit mGluR5 in key paralimbic areas as a strong determinant of the temperament trait novelty seeking. These data add to our understanding of how brain neurochemistry accounts for the variation in human behavior and strongly support further research on mGluR5 as a potential therapeutic target in neuropsychiatric disorders associated with abnormal novelty-seeking behaviors.
Decrease of mGluR5 receptor density goes parallel with changes in enkephalin and substance P immunoreactivity in Huntington's disease
The metabotropic glutamate receptor subtype 5 (mGluR5) has been implicated in the pathophysiology of mood and anxiety disorders.
The interaction between GRM5 and cellular prion protein has a central role in transgenic mouse model of Alzheimer's disease pathogenesis.
Data suggest that metabotropic glutamate receptors recycling is completely dependent on the activity of PP2A whereas, PP2B has partial effect on this process.
findings provide evidence for decreased expression of metabotropic glutamate receptor 5 and its signaling components representing a key pathophysiological hallmark in autism spectrum disorder.
Study provided evidence that protein expression of mGluR5 is significantly higher (total: 42%; monomer: 25%; dimer: 52%) in the hippocampal CA1 region of schizophrenia subjects relative to healthy controls
Results provide compelling evidence that mGluR5 regulation is altered in schizophrenia, likely contributing to the altered glutamatergic signaling that is associated with the disorder
This review supports altered mGluR5 functioning as a convergent point in ASD pathogenesis and indicates more research is warranted into mGluR5 as a potential therapeutic target.
both an increased and reduced mGlu5 functioning seem to be associated with Intellectual Disability and autism spectrum disorders.
Findings suggest that mGluR2/3 and mGluR5s are unaltered in the anterior cingulate cortex in psychotic and nonpsychotic depression, bipolar disorder and schizophrenia
Our results demonstrated that mGluR5-mediated short-term plasticity in the anterior cingulate cortex may be a critical mechanism for chronic pain
the role of mGluR5 in dopamine receptor 1-containing neurons in dyskinesia, is reported.
under conditions of low stress, mGluR5 Knockout mice exhibit a pronounced perseverative phenotype that blunts cognitive flexibility.
findings provide the molecular evidence for how targeting mGluR5 using a well-tolerated selective NAM can mitigate two critical mechanisms of neurodegeneration, autophagy and apoptosis.
Manipulating the levels of Gprasp2 bidirectionally modulates the surface availability of mGluR5 and produces alterations in dendritic complexity, spine density and synaptic maturation.
In a mouse moderate traumatic brain injury model, the authors found that mGluR5 knockout (KO) significantly reduced neutrophil infiltration and inflammatory cytokine expression in the brain at 24 hours post injury, which was accompanied by improved neurological dysfunction.
Results demonstrate that inhibition of mGluR5 corrects hyperactivity, seizures, and elevated de novo synaptic protein synthesis. Conversely, positive allosteric modulation of mGluR5 results in the exacerbation of hyperactivity and epileptic phenotypes. The data suggest a meaningful therapeutic potential for mGluR5 negative allosteric modulators in tuberous sclerosis complex.
these results reveal a critical period in adolescence during which social isolation can induce anxiety behaviors and facilitate basolateral amygdala pyramidal neuronal excitability, both of which are mediated by mGluR5.
Describe a complete knockout mouse model of the autism-associated Shank3 gene, with a deletion of exons 4-22 (Deltae4-22). Both mGluR5-Homer scaffolds and mGluR5-mediated signalling are selectively altered in striatal neurons. These changes are associated with perturbed function at striatal synapses, abnormal brain morphology, aberrant structural connectivity and autism spectrum disorder-like behaviour.
Study identified an unexpected age-linked recovery of synaptic gain function in Fragile X syndrome (FXS) model mice medial prefrontal cortex. Stimulus evoked long-term depression mediated by endocannabinoids, absent in early adulthood (2-month-old), is recovered with senescence (at 1-year-old); recovery depends on the engagement of alternative mGlu5 coupled mechanisms.
Study shows that blocking of metabotropic glutamate type 5 receptor (mGlu5) reduced the dysregulation of glutamate transmission and improved motor coordination in the Grm1crv4 mouse model of cerebellar ataxia SCAR13.
The authors here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis.
mGluR5 was significantly more mobile at synapses in hippocampal Fmr1 KO neurons, causing an increased synaptic surface co-clustering of mGluR5 and NMDAR.
Results support positive allosteric modulation of mGlu5, particularly with VU0409551, as a viable mechanism to reverse the deficits in NMDA receptor function, synaptic plasticity, and memory that are known to be impaired in schizophrenia.
Collectively, these results indicate that selective antagonism of glutamate and mGluR5 has a potentially beneficial effect in both liver cancer and Parkinson's disease, and thus may provide more understanding for the clinical investigation and further an additional therapeutic target for these two diseases.
beta-arrestin2-biased negative modulators of mGlu5 offer significant advantages over first-generation inhibitors for the treatment of fragile X and related disorders.
mGluR5 and CB1 act in concert to activate neuroprotective cell signaling pathways and promote neuronal survival.
This study confirmed the presence of mGluR1/5 complex by (i) reverse immunoprecipitation using an mGluR1 antibody to pulldown mGluR5 from hippocampal tissue.
Here, we show in a mouse model of Rett syndrome (Mecp2 KO) that metabotropic glutamate receptor 5 (mGluR5)- and protein-synthesis-dependent synaptic plasticity are abnormal in the hippocampus.
In a mouse model mimicking n-3 PUFA dietary deficiency during adolescence and adulthood, we found strong increases in anxiety and anhedonia which lead to decreases in specific cognitive functions in adulthood. We found that endocannabinoid/mGlu5-mediated LTD and NMDAR-dependent LTP were lacking in adult n-3-deficient 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. Multiple transcript variants encoding different isoforms have been found for this gene.
metabotropic glutamate receptor 5
, metabotropic glutamate receptor 5 variant F
, metabotropic glutamate receptor 5 variant G
, metabotropic glutamate receptor 5 variant H
, metabotropic glutamate receptor (mGluR5)
, metabotropic glutamate receptor 5b
, G protein coupled receptor, family C, group 1, member E
, G protein-coupled receptor GRM5
, G protein-coupled receptor, family C, group 1, member E
, metabotropic glutamate receptor subtype 5b
, metabotropic glutamate receptor type 5