Description
Product Characteristics: FUNCTION: Transports L-glutamate and also L- and D-aspartate. Essential for terminating the postsynaptic action of glutamate by rapidly removing released glutamate from the synaptic cleft. Acts as a symport by cotransporting sodium. Negatively regulated by ARL6IP5. Defects in SLC1A1 may be a cause of dicarboxylicamino aciduria, also known as glutamate-aspartate transport defect. This is as defect in renal and probably intestinal transport of glutamic and aspartic acids and is associated with moderate hyperprolinemia. SUBCELLULAR LOCATION: Membrane, Multi-pass membrane protein. TISSUE SPECIFICITY: Expressed in all tissues tested including liver, muscle, testis, ovary, retinoblastoma cell line, neurons and brain (in which there was dense expression in substantia nigra, red nucleus, hippocampus and in cerebral cortical layers).,SLC1 Family,Sodium-dependent glutamate/aspartate transporter 3, Excitatory amino-acid carrier 1, Neuronal and epithelial glutamate transporter, Solute carrier family 1 member 1, EAAC1, EAAT3, SLC1A1
Target Information: 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. [provided by RefSeq, Mar 2010]