Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human GRID2 Anticorps:
anti-Mouse (Murine) GRID2 Anticorps:
anti-Rat (Rattus) GRID2 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
These results suggest that the expression of zebrafish GluRdelta2 is selective for cerebellum-like neural wiring with large numbers of parallel fiber inputs.
Report on a consanguineous family with autosomal recessive childhood onset of cerebellar ataxia and delayed psychomotor development. Using whole exome sequencing we identified a novel homozygous missense variant [c.2128C > T, p.(Arg710Trp)] in GRID2 that segregates with the disease. The missense variant is located in a conserved region encoding the extracellular serine-binding domain of the GluD2 protein.
GRID2 gene can be a suppressor in TNF-induced neurodegeneration which may help to understand the main factors leading to autism.
Glutamate system genes including have been associated with disease risk in recent analyses from the Psychiatric Genomics Consortium.
findings suggest a possible role of GRID2 in the susceptibility to develop mevalonate kinase deficiency. GRID2 gene associated with MKD: The rs1450500 SNP was differently distributed in patients with MKD with respect to those with recurrent fever.
We demonstrated for the first time GRID2 expression and localization in human and murine retina, providing evidence for a novel functional role of GRID2 in the retina.
GRID2 point mutations: cerebellar ataxia is the core phenotype, but with variable severity ranging from very mild adult-onset to congenital-onset linked to both the heterozygous and homozygous state of the variant, and the position of the mutation.
GluD2 gating is triggered by type 1 metabotropic glutamate receptors.
GRID2 mutations are associated with a recessive syndrome causing cerebellar ataxia and eye movement abnormalities.
Tests for gene-environment interaction between these 33 genes and maternal smoking found evidence for interaction with two additional genes: GRID2 and ELAVL2 among European mothers
Glutamate receptor delta2 is involved in a common mechanism that restricts the number of synaptic AMPA receptors at parallel fiber synapses in cerebellar Purkinje cells.
Thus, phosphorylation of -2T and/or -1S of GluRdelta2 C-terminus by PKA may regulate the binding of GluRdelta2 to its scaffolding protein, Delphilin.
The carboxy terminus of transgenic GluRdelta2 conveys the signal(s) necessary for long-term depression induction and motor learning.
GLUD2 transgenic mice were generated by inserting in their genome, a segment of the human X chromosome containing the GLUD2 gene and its promoter.
Results suggest that the GluRdelta2 receptor plays an important role in the long-term organization of the granule-Purkinje cell circuit through its involvement in the regulation of parallel fiber-Purkinje cell synaptogenesis and in the normal functioning of this critical cerebellar circuit.
The GluD2 mutation in the ho15J mice affects stable retention of the acquired conditioned bradycardia.
Notably, the introduction of GLUD2 did not affect glutamate levels in mice, consistent with observations in the primates. Instead, the metabolic effects of GLUD2 center on the tricarboxylic acid cycle, suggesting that GLUD2 affects carbon flux during early brain development, possibly supporting lipid biosynthesis.
This study showed that spontaneous Grid2 mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
Established is a mouse line with an autosomal recessive gene mutation characterized by progressive ataxia and significant cerebellar atrophy.
GluD2 works in concert with GluD1 for the construction of cerebellar synaptic wiring through distinct neuronal and synaptic expressions.
Climbing fiber signals in Glu2 receptor delta2 knock-out mice propagate across multiple microzones.
GluD2 deletion impairs presynaptic R-type voltage-gated Ca(2+) channels, resulting in decreased release of synaptic vesicles
The results suggest that multiple PC death pathways are induced by the physical trauma of making organotypic slice cultures, naturally-occurring postnatal cell death, and the GluRdelta2 (Lc) mutation.
CD95 and soluble CD95L contribute, via non-apoptotic signaling, to the inflammatory reaction initiated early in neuron death within the Grid2(Lc/+) cerebellum
activity-dependent phosphorylation of serine 880 (S880) in GluA2 AMPA receptor subunit, which is an essential step for AMPA receptor endocytosis during LTD induction, was impaired in GluD2-null cerebellum
GluRdelta2 is part of the mGluR1 signaling complex needed for cerebellar synaptic function and motor coordination
[review] The Cbln1-GluRdelta2 receptor complex is located at the cleft of parallel fiber-Purkinje cell synapses and bidirectionally regulates both presynaptic and postsynaptic differentiation.
[review] GluRdelta2 plays critical roles in formation, maturation, and/or maintenance of granule neuron-Purkinje neuron synapses.
These results indicate that glial D-Ser regulates synaptic plasticity and cerebellar functions by interacting with GluD2.
It is a molecule involved in synaptic plasticity in the cerebellum. (review)
GluRdelta2 fuels heterosynaptic competition and gives purkinje fibers the competitive advantages over climbing fibers throughout the animal's life.
Results suggest that GluRdelta2 mediates cerebellar synapse formation by interacting with presynaptic NRXNs through Cbln1.
study found that Cbln1 binds directly to the N-terminal domain of glutamate receptor delta2 (GluD2); results indicate that the Cbln1-GluD2 complex is a unique synapse organizer that acts bidirectionally on both pre- and postsynaptic components
Human glutamate receptor delta-2 (GRID2) is a relatively new member of the family of ionotropic glutamate receptors which are the predominant excitatory neurotransmitter receptors in the mammalian brain. GRID2 is a predicted 1,007 amino acid protein that shares 97% identity with the mouse homolog which is expressed selectively in cerebellar Purkinje cells. A point mutation in mouse GRID2, associated with the phenotype named 'lurcher', in the heterozygous state leads to ataxia resulting from selective, cell-autonomous apoptosis of cerebellar Purkinje cells during postnatal development. Mice homozygous for this mutation die shortly after birth from massive loss of mid- and hindbrain neurons during late embryogenesis. This strongly suggests a role for GRID2 in neuronal apoptotic death.
gluR delta-2 subunit
, glutamate receptor delta-2 subunit
, glutamate receptor ionotropic, delta-2
, glutamate receptor, ionotropic, delta 2
, glutamate receptor delta-2 subunit-like
, minisatellite 10ac detected by probe MMS10