High impact information on SLC1A1

• Na(+)-dependent transporters for glutamate exist on astrocytes (EAAT1 and EAAT2) and neurons (EAAT3) [1].
• The relative activity of the three transporters was found to be approximately 1:3:6 for EAAT1, EAAT2, and EAAT3, respectively [1].
• Na(+)-dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) of the blood-brain barrier. A mechanism for glutamate removal [1].
• Inhibition of glutamate transport was observed using inhibitors specific for EAAT2 (kainic acid and dihydrokainic acid) and EAAT3 (cysteine) [1].
• This effect is dependent on protein synthesis and glycosylation and is accompanied by an increase in EAAC1 mRNA levels [2].

Anatomical context of SLC1A1

• Regulation of the glutamate transporter by amino acid deprivation and associated effects on the level of EAAC1 mRNA in the renal epithelial cell line NBL-I [3].
• In addition, EAAC1 was present in a small population of cells that are probably adult oligodendrocyte progenitor cells [4].
• The presence and distribution of the glutamate transporters, EAAC1, GLAST and GLT-1, were examined in the adult bovine corpus callosum by means of Western blotting and immunohistochemistry [4].

Associations of SLC1A1 with chemical compounds

• Conversely, the induction of high affinity glutamate transport by hyperosmotic shock was accompanied by an increase in EAAC1 protein [5].

Analytical, diagnostic and therapeutic context of SLC1A1

• Western blotting using antibodies to the C-terminal region of EAAC1 showed that there is no increase in the amount of EAAC1 protein on prolonged incubation in amino acid-free medium [5].

References