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Our study showed a lack of association between SLC1A1 variants and normal tension glaucoma in Japanese patients, suggesting that the SLC1A1 gene does not play a critical role in the development of the disorder in this patient population.
Numb (show NUMB ELISA Kits) is a pivotal adaptor protein that mediates the subcellular localization of EAAT3 through binding the YxNxxF (where x stands for any amino acid) motif.
observations provide insights into the molecular basis of hot water epilepsy and show the role of SLC1A1 variants in this intriguing neurobehavioral disorder
This study demonstrated that Variations within SLC1A1 are associated with risk of epileptogenesis following posttraumatic brain injury.
Lithium-sensitive GSK3ss is a powerful regulator of excitatory amino acid transporters EAAT3 and EAAT4 (show SLC1A6 ELISA Kits).
Data suggest that EAAC1 transporters present on NST (show SULT4A1 ELISA Kits) dendrites may play a minor role if any in glutamate (show GRIN1 ELISA Kits) clearance.
SPAK (show STK39 ELISA Kits) and OSR1 (show OXSR1 ELISA Kits) are negative regulators of EAAT3 activity
Excitatory amino acid carrier 1 (EAAC1) plays a pivotal role in neuronal glutathione synthesis to maintain cellular redox homeostasis.
Transport of either L-glutamate (show GRIN1 ELISA Kits) or L-selenocysteine by EAAT3 decreased intracellular pH, whereas transport of cysteine resulted in cytoplasmic alkalinization.
variability within the SLC1A1 gene impacts both the presence and severity of posttraumatic stress disorder among a sample of combat-exposed veterans.
Morphine increased EAAT3 expression in the plasma membrane of medial prefrontal cortex, nucleus accumbens and ventral tegmental area but did not affect EAAT3 expression in the hippocampus. Results also suggest that EAAT3 delays the extinction of morphine-induced conditioned place preference (CPP). EAAT activation may prevent the formation of morphine-induced CPP.
partial loss of the Slc1a1 gene in mice causes haploinsufficiency associated with behavioral, histological and biochemical changes that reflect an altered redox state and may promote the expression of behavioral features and inflammatory states consistent with those observed in schizophrenia.
this paper shows increased EAAC1 protein expression in lysates from livers of NOD mice compared with B6 mice
These findings suggest that cysteine uptake by EAAC1 is important for neuronal antioxidant function under ischemic conditions.
these studies indicate that absence of EAAC1 results in either a decrease in pilocarpine-induced seizures that is not detectable by behavioral criteria
EAAT3 is upstream of PKA in a pathway to regulate GluR1 (show GRIA1 ELISA Kits) trafficking.
EAAT3/EAAC1 expression is altered in murine models of human neurodegenerative diseases. (Review)
These results suggest that the isoflurane preconditioning-induced acute phase of neuroprotection involves EAAT3.
These findings indicate that regulation of heart rate, a vital sign, is one of the EAAT (show SLC1A2 ELISA Kits) biological functions.
Study implicates EAAC1-dependent cysteine uptake as an endogenous source of enhancing antioxidant function and zinc homeostasis in neurons in the ischemic brain.
Data suggest that expression of SLC1A1 in intestinal epithelial cells can be regulated by dietary components; expression of SLC1A1 is up-regulated by L-glutamate (show GRIN2C ELISA Kits), an abundant dietary amino acid and dietary supplement.
These findings indicate that the expression of the EAAC1 in jejunum is much depending on the stage of piglet development and that low BW at birth is associated with lower expression of this carrier in the early suckling period.
Glutamate (show GRIN2C ELISA Kits) uptake across apical membrane is regulated by changing expression of EAAC-1 at transcription and translation levels as well as maximal uptake activity and transporter affinity along the intestinal crypt-villus axis in the neonate.
This study is focused on the assessment of non-exocytotic glutamate (show GRIN2A ELISA Kits) release, that is, the unstimulated release, heteroexchange and glutamate transporter reversal in platelets.
This gene encodes a member of the high-affinity glutamate transporters that play an essential role in transporting glutamate across plasma membranes. In brain, these transporters are crucial in terminating the postsynaptic action of the neurotransmitter glutamate, and in maintaining extracellular glutamate concentrations below neurotoxic levels. This transporter also transports aspartate, and mutations in this gene are thought to cause dicarboxylicamino aciduria, also known as glutamate-aspartate transport defect.
excitatory amino acid transporter 3
, excitatory amino acid carrier 1
, neuronal and epithelial glutamate transporter
, sodium-dependent glutamate/aspartate transporter 3
, solute carrier family 1 member 1
, excitatory amino acid carrier 2
, excitatory amino-acid carrier 1
, glutamate transporter mEAAC2
, solute carrier family 1, member 1
, Solute carrier family 1 A1 (brain glutamate transporter)
, excitatory amino acid transporter-3
, glutamate transporter
, renal high affinity glutamate transporter EAAC1
, high-affinity glutamate transporter