Anti-EAAT1 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

EAAT1 also known as Excitatory Amino Acid Transporter 1 or anti-GLAST plays a critical role in mediating the uptake of glutamate from the synaptic cleft into glial cells. This transporter helps maintain the delicate balance of excitatory neurotransmission in the central nervous system. EAAT1 has a molecular mass of approximately 57 kDa. You will find EAAT1 expressed predominantly in astrocytes within the brain and retina where it facilitates the regulation of extracellular concentrations of glutamate preventing excitotoxicity.

Biological function summary

EAAT1 is instrumental in maintaining low levels of extracellular glutamate acting as a protective mechanism against neurotoxicity. This transporter does not operate as part of a larger protein complex instead functioning independently to efficiently clear synaptic glutamate. By ensuring rapid uptake of glutamate EAAT1 helps maintain normal synaptic transmission and neuronal communication. The action of EAAT1 is important for preventing excessive activation of glutamate receptors which can lead to cellular damage.

Pathways

EAAT1 is heavily involved in the glutamatergic neurotransmission pathway which is essential for various brain functions including learning and memory. EAAT1 acts in coordination with other proteins like EAAT2 to manage glutamate levels within the synaptic cleft. Another pathway where EAAT1 plays a role is the glutamate-glutamine cycle where it works alongside proteins such as glutamine synthetase to recycle glutamate and sustain neurotransmitter balance. This interplay supports neuronal health and protects against glutamate excitotoxicity.

Associated diseases and disorders

EAAT1 has been implicated in neurological conditions such as epilepsy and Alzheimer's disease. The dysfunction or altered expression of EAAT1 can lead to insufficient glutamate clearance contributing to the pathophysiology of these disorders. In epilepsy the decreased function of EAAT1 may result in abnormally high levels of synaptic glutamate enhancing the risk of seizures. Similarly in Alzheimer's altered EAAT1 activity can exacerbate neurodegenerative processes. EAAT1's role is tightly linked with proteins like NMDA receptors and EAAT2 which further influence disease progression by affecting glutamate dynamics.