Solute Family 1, member 3 (SLC1A3) is a protein that, in humans, is encoded by the SLC1A3 gene. SLC1A3 is a glial high-affinity glutamate transporter. SLC1A3 is commonly referred to as glutamate aspartate transporter (GLAST) or excitatory amino acid transporter 1 (EAAT1). SLC1A3 is primarily expressed in the serosa, enabling it to remove glutamate from the extracellular space. It is also localized in the mitochondrial membrane as part of the malate-aspartate shuttle.
Basic Information of SLC1A3 | |
Protein Name | Excitatory amino acid transporter 1 (EAAT1) |
Gene Name | SLC1A3 |
Aliases | Sodium-dependent glutamate/aspartate transporter 1 (GLAST-1), Solute carrier family 1 member 3 |
Organism | Homo sapiens (Human) |
UniProt ID | P43003 |
Transmembrane Times | 8 |
Length (aa) | 542 |
Sequence | MTKSNGEEPKMGGRMERFQQGVRKRTLLAKKKVQNITKEDVKSYLFRNAFVLLTVTAVIVGTILGFTLRPYRMSYREVKYFSFPGELLMRMLQMLVLPLIISSLVTGMAALDSKASGKMGMRAVVYYMTTTIIAVVIGIIIVIIIHPGKGTKENMHREGKIVRVTAADAFLDLIRNMFPPNLVEACFKQFKTNYEKRSFKVPIQANETLVGAVINNVSEAMETLTRITEELVPVPGSVNGVNALGLVVFSMCFGFVIGNMKEQGQALREFFDSLNEAIMRLVAVIMWYAPVGILFLIAGKIVEMEDMGVIGGQLAMYTVTVIVGLLIHAVIVLPLLYFLVTRKNPWVFIGGLLQALITALGTSSSSATLPITFKCLEENNGVDKRVTRFVLPVGATINMDGTALYEALAAIFIAQVNNFELNFGQIITISITATAASIGAAGIPQAGLVTMVIVLTSVGLPTDDITLIIAVDWFLDRLRTTTNVLGDSLGAGIVEHLSRHELKNRDVEMGNSVIEENEMKKPYQLIAQDNETEKPIDSETKM |
SLC1A3 is an isoform in the body. SLC1A3 regulates the transport of glutamate and aspartic acid with reverse transport of 3 Na+ and 1 H+ cation and 1 K+ cation. This joint transport coupling (or symport) allows the transfer of glutamate into the cell to counter the concentration gradient. It is associated with type 6 ataxia. Dl-3-beta-benzyloxyaspartate (TBOA) is an inhibitor of excitatory amino acid transporters. A selective inhibitor of SLC1A3 was recently discovered, based on 25 combinations of substitutions, 2-amino-5-oxo-5,6,7,8-tetrahydro-chromium-3-carbonyl at 4 and 7 positions.
Fig.1 The structure of SLC1A3 Protein.
This is the first study of clinically relevant vertebral osteoporosis phenotypes for linkSLC1A3 and EPHB2. These results may help elucidate vertebral biology and new ways to reduce the incidence of vertebral fractures.
This article shows that SLC1A3-CreER is also induced in hydrogen fluoride in anagen, and reports the pattern of labeling produced during the different stages of TBIL, further examining its role as a niche and its crosstalk with high-frequency stem cells.
These findings support the fact that Hypoxia-Inducible Factors regulate SLC1A1 and SLC1A3 gene expression in hypoxic Hep3B cells.
These findings extend the phenotype profile of the SLC1A3 gene variant, and imply that the impaired K+ binding with hEAAT1 may be a new mechanism of glutamate transport dysfunction in human disease.
The results reveal that on the messenger RNA and protein levels, the anti-inflammatory effects of fingolimod may restore the reduced expression of SLC1A2 and SLC1A3.
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