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anti-Human GRID2 Anticorps:
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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 (Montrer GLUD2 Anticorps) protein.
GRID2 gene can be a suppressor in TNF (Montrer TNF Anticorps)-induced neurodegeneration which may help to understand the main factors leading to autism.
Glutamate (Montrer GRIN1 Anticorps) 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 (Montrer MVK Anticorps) 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 (Montrer GLUD2 Anticorps) gating is triggered by type 1 metabotropic glutamate (Montrer GRIN1 Anticorps) 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 (Montrer ELAVL2 Anticorps) among European mothers
Glutamate (Montrer GRIN1 Anticorps) receptor delta2 is involved in a common mechanism that restricts the number of synaptic AMPA (Montrer GRIA3 Anticorps) receptors at parallel fiber synapses in cerebellar Purkinje cells.
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 (Montrer GLUD2 Anticorps) mutation in the ho15J mice affects stable retention of the acquired conditioned bradycardia.
Notably, the introduction of GLUD2 (Montrer GLUD2 Anticorps) did not affect glutamate (Montrer GRIN1 Anticorps) levels in mice, consistent with observations in the primates. Instead, the metabolic effects of GLUD2 (Montrer GLUD2 Anticorps) center on the tricarboxylic acid cycle, suggesting that GLUD2 (Montrer GLUD2 Anticorps) 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 (Montrer GLUD2 Anticorps) works in concert with GluD1 (Montrer GLUD1 Anticorps) 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 (Montrer GLUD2 Anticorps) deletion impairs presynaptic R-type voltage-gated Ca(2 (Montrer CA2 Anticorps)+) 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 (Montrer FAS Anticorps) and soluble CD95L (Montrer FASL Anticorps) contribute, via non-apoptotic signaling, to the inflammatory reaction initiated early in neuron death within the Grid2(Lc/+) cerebellum
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