SLC1A3

(redirected from EAAT1)

SLC1A3

A gene on chromosome 5p13 that encodes solute carrier family 1 member 3, a high-affinity glutamate transporter that plays a key role in transporting glutamate across plasma membranes. In the brain, these transporters clear the excitatory neurotransmitter glutamate from the extracellular space at synapses in the CNS and maintain extracellular glutamate concentrations below neurotoxic levels.
 
Molecular biology
SLC1A3 mutations are associated with episodic ataxia, Type 6.
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Decreased expression of KIF1A motor proteins, presynaptic proteins, glutamate receptors, the glutamate transporter EAAT1 and 2, and CaM kinase II was noted in MS brains compared to those of controls [34].
Other proteins expressed by astrocytes such as connexin 30 and 43 (gap junction proteins), the water channel aquaporin-4 (AQP4), the calcium-binding protein S100[beta] and the amino acid transporters 1 and 2 (EAAT1, EAAT2), and glutamine synthetase have altered expression levels in both animals models of stress and in human brain samples analyzed postmortem compared with controls (reviewed in [89]).
Additional biochemical examination showed that the [Per2.sup.Brdm1] mutant mice had a deletion in the PAS domain of the Per2 protein that resulted in reduced glutamate transporter Eaat1 expression levels and in turn increased synaptic glutamate levels.
Zaragoza et al., "[Na.sup.+] dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) in primary astrocyte cultures: effect of oxidative stress," Brain Research, vol.
The invention is directed toward the isolation, characterization and pharmacological use of the human amino acid transporter proteins EAAT1, EAAT2, EAAT3 and ASCT1.
Downregulation of GJ proteins Cx43 and Cx30, inwardly rectifying [K.sup.+] channels (Kir4.1), the glial excitatory amino acid transporters (EAAT1 and EAAT2), and dislocation of aquaporins (AQP4), represents astrocyte activation induced by BBB disruption, as well as by focal application of albumin or TGF-[beta].
WDR62 expression was then significantly reduced at the end of neural induction (ANOVA, P < 5.0E - 03, n = 5) and also at the NSP stage (aNOVA, P < 5.0E - 03, n = 5), which corresponded with an increase in expression of TBR2, TUJ1, EAAT1, and S100[beta] (Figure 1(f)).
This was accompanied by significantly increased expression of PAX6 (twotailed t-test, P = 0.01, n = 3) and functional glial marker EAAT1 (two-tailed t-test, P = 0.04, n = 3) (Figure 5).
In contrast, treatment with JNK-specific inhibitor increased WDR62 expression in hPSC-derived neural progenitors and this coincided with enhanced expression of PAX6-positive cells and astrocyte functional marker EAAT1. Thus, our findings indicate that JNK activity may also negatively regulate the expression levels of WDR62.
(f) Gene expression analyses of pluripotency marker OCT4; neural progenitor markers SOX2, PAX6, and TBR2; neuronal marker TUJ; glial markers EAAT1 and S100[beta]; and proliferative marker KI67 and WDR62 across several time points of the neural induction protocol, including hPSC, day 7 NI, day 14 NI, and 1-week NSPs (n > 4 independent experiments for each time point, >3 NSPs per experiment).