Slc1A2 — Solute Carrier Family 1 Member 2 is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| Gene Information | |
|---|---|
| Symbol | SLC1A2 |
| Full Name | Solute Carrier Family 1 Member 2 (EAAT2/GLT-1) |
| Chromosome | 11 |
| NCBI Gene ID | 6506 |
| OMIM | 600670 |
| UniProt ID | Q15029 |
| Ensembl ID | ENSG00000178176 |
SLC1A2 (also known as EAAT2 or GLT-1) is the major glutamate transporter in the brain, responsible for clearing glutamate from the synaptic cleft and preventing excitotoxicity. It is implicated in ALS, Alzheimer's disease, and stroke. Reduced EAAT2 expression and function contribute to excitotoxic neuronal death.
SLC1A2/EAAT2 is a sodium-dependent glutamate transporter that clears glutamate from the extracellular space. It couples glutamate uptake to sodium and potassium gradients. EAAT2 is the predominant glutamate transporter in the brain, accounting for over 90% of glutamate uptake capacity.
Highly expressed in astrocytes, particularly around synapses.
| Disease | Role in Disease |
|---|---|
| ALS | Glutamate uptake deficiency, excitotoxicity, motor neuron death |
| Alzheimer's Disease | Excitotoxic mechanisms, Aβ effects on glutamate transport |
| Stroke | Ischemic excitotoxicity, glutamate transporter dysfunction |
| Parkinson's Disease | Dopaminergic neuron vulnerability, excitotoxicity |
SLC1A2 (Solute Carrier Family 1 Member 2), also known as EAAT2 (Excitatory Amino Acid Transporter 2), is the primary glutamate transporter in the brain. It clears glutamate from the synaptic cleft, preventing excitotoxicity.
SLC1A2:
| Approach | Strategy | Status |
|---|---|---|
| CElli-101 | Gene therapy (AAV-EAAT2) | Clinical trials |
| Small molecule enhancers | Increase expression | Research |
SLC1A2 (EAAT2) is the dominant glutamate transporter in the brain, expressed primarily in astrocytes with highest expression in hippocampus and cortex. It is responsible for more than 90% of glutamate uptake.
EAAT2 transports glutamate into astrocytes, preventing excitotoxicity through an electrogenic transport mechanism.
EAAT2 function is coupled to the glutamate-glutamine cycle.
EAAT2 expression and function are reduced in AD, contributing to excitotoxicity (PubMed: 10077666).
EAAT2 dysfunction is a key mechanism in ALS. Mutations in SLC1A2 cause ALS (PubMed: 21458745).
EAAT2 reversal during ischemia causes glutamate release and excitotoxic cell death.
EAAT2 activators (CEI-1040, T-588), gene therapy (AAV-EAAT2), and ceftriaxone upregulating EAAT2 expression are being investigated.
The study of Slc1A2 — Solute Carrier Family 1 Member 2 has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
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