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Data suggest that EAAT2 functions as a taurine transporter in vivo and is physiologically required for the sensory perception of specific environmental molecules.
Taurine and aspartate are transported with similar K(m) and relative efficacy and behave as mutually competitive inhibitors; dEAAT2 is actually an aspartate/taurine transporter
This study provides further evidence for SLC1A2 mutations in epileptic encephalopathies and suggests a gain-of-function mechanism for this rather severe presentation.
GLT1 was demonstrated by luciferase assay to be a target of miR (show MLXIP Proteins)-31-5p and miR (show MLXIP Proteins)-200c-3p, and both its mRNA and protein (immunohistochemistry) significantly decreased with age in liver biopsies and in hepatic centrilobular zone, respectively
Mutations in SLC1A2 and CACNA1A (show CACNA1A Proteins) Are Important Causes of Epileptic Encephalopathies
The results of this study suggested SLC1A2 rs3794087 may decrease the risk for Parkinson's disease in a Chinese cohort, but do not support a role in the susceptibility to amyotrophic lateral sclerosis or multiple system atrophy.
that Abeta1-42 oligomers could cause disturbances in insulin (show INS Proteins)/Akt (show AKT1 Proteins)/EAAT signaling in astrocytes
This study showed a lack of association between of SLC1A2 rs3794087 with the risk for essential tremor.
Results suggest that genetic variation (rs4354668 and its haplotypes) in SLC1A2 may be involved in impaired executive function, which adds to the current body of knowledge regarding the risk of schizophrenia and the impairment of cognitive performance
SPAK (show STK39 Proteins) and OSR1 (show OXSR1 Proteins) are powerful negative regulators of the excitatory glutamate (show GRIN1 Proteins) transporters EAAT1 (show SLC1A3 Proteins) and EAAT2.
PPARgamma (show PPARG Proteins) agonist pioglitazone has a role in modulating EAAT2 expression in glioma cells
Two recurrent SLC1A2 missense variants and one recurrent 5'-untranslated region variant were found to be associated with susceptibility to the development of bipolar disorder and schizophrenia.
Mutation of the caspase-3 (show CASP3 Proteins) cleavage site in the astroglial glutamate transporter (show SLC1A1 Proteins) EAAT2 delays disease progression and extends lifespan in the SOD1 (show SOD1 Proteins)-G93A mouse model of amyotrophic lateral sclerosis
The upregulation of GLT-1 induced by transplanted neural precursor cells was found to rely on the secretion of VEGF by neural precursor cells
We demonstrate that the R6/1 transgenic mouse model of HD has lower basal levels of cystine, and showed depressive-like behaviors in the forced-swim test. Administration of NAC reversed these behaviors. This effect was blocked by co-administration of the system xc(-) and GLT-1 inhibitors CPG and DHK, showing that glutamate transporter activity was required for the antidepressant effects of NAC
Consistent with glutamate (show GRIN1 Proteins) dysregulation, analysis of neurons reveal changes in morphology including a reduction in dendritic spines, VGlut1 and NeuN (show RBFOX3 Proteins) immunoreactivity
A significant initial increase in dorsal hippocampal GLT1 immunoreactivity and protein levels were observed 1day post epilepsy and followed by a marked downregulation at 4 and 7days post epilepsy with a return to near control levels by 30days post epilepsy.
These results demonstrate that focal restoration of GLT1 expression in the superficial dorsal horn is a promising target for treating chronic neuropathic pain following SCI.
Lipid raft integrity, ensured by DHCR24 (show DHCR24 Proteins), plays a crucial role in the ischemic brain by guaranteeing EAAT2-mediated uptake of glutamate (show GRIN1 Proteins) excess.
Findings suggest that focal restoration of glutamate transporter (show SLC1A1 Proteins) 1,expression in astrocytes of the cervical spinal cord using adeno (show ADORA2A Proteins)-associated virus delivery is not an effective therapy for amyotrophic lateral sclerosis.
we have demonstrated for the first time that DOR receptor activation induces astrocytic expression of EAAT1 (show SLC1A3 Proteins) and EAAT2
neuronal GLT-1 but not astrocytic GLT-1 contributed significantly to glutamate uptake. astrocytic GLT-1 performs critical functions required for normal weight gain, resistance to epilepsy, and survival.
Disruption of Eaat2b, a glutamate transporter (show SLC1A1 Proteins), results in abnormal motor behaviors in developing zebrafish.
This gene encodes a member of a family of solute transporter proteins. The membrane-bound protein is the principal transporter that clears the excitatory neurotransmitter glutamate from the extracellular space at synapses in the central nervous system. Glutamate clearance is necessary for proper synaptic activation and to prevent neuronal damage from excessive activation of glutamate receptors. Mutations in and decreased expression of this protein are associated with amyotrophic lateral sclerosis. Alternatively spliced transcript variants of this gene have been identified.
, excitatory amino acid transporter 2
, sodium-dependent excitatory amino acid transporter 2
, glutamate transporter Am-EAAT
, solute carrier family 1 (glial high affinity glutamate transporter), member 2
, excitatory amino acid transporter 2-like
, high affinity glucose transporter
, sodium-dependent glutamate/aspartate transporter 2
, excitotoxic amino acid transporter 2
, glutamate/aspartate transporter II
, glial high affinity glutamate transporter
, solute carrier family 1 member 2
, solute carrier family 1, member 2
, glutamate transporter