Anti-EAAT5 antibody

Supplementary info

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

Activity summary

EAAT5 also known as Excitatory Amino Acid Transporter 5 or SLC1A7 is a protein involved in transporting the neurotransmitter glutamate across cell membranes. It functions as a glutamate transporter and chloride channel helping regulate glutamate concentrations in the synaptic cleft and maintaining electrical balance in retinal cells. EAAT5 shows expression mainly in the retina and also present in other parts of the central nervous system. The mass of EAAT5 is approximately 60 kDa. This protein belongs to the family of excitatory amino acid transporters which play an important role in synaptic signaling.

Biological function summary

EAAT5 mediates glutamatergic neurotransmission by removing excess glutamate from the synaptic cleft reducing excitotoxicity and maintaining synaptic plasticity. The function of EAAT5 is critical in visual processing as it plays a role in signal transmission in the retina. It operates as part of a complex that involves various neurotransmitter transporters and channels ensuring precise communication between photoreceptor cells and downstream neurons. The transport activity of EAAT5 impacts neurotransmitter gradients influencing visual perception and adaptation to light changes.

Pathways

EAAT5 participates in the glutamatergic signaling pathway where it helps modulate synaptic transmission by controlling extracellular glutamate levels. It is functionally related to other members of the excitatory amino acid transporter family such as EAAT1 and EAAT2 which also manage glutamate reuptake in the central nervous system. The protein's interplay in the regulation of glutamate impacts neural activities and is associated with the Catabolism of Glutamate pathway. These transporters work together to ensure glutamate does not accumulate to toxic levels safeguarding neurons from damage.

Associated diseases and disorders

Disturbances in EAAT5 function have been linked to retinal disorders particularly those involving night vision impairment. Abnormal expression or malfunction of EAAT5 can contribute to excitotoxicity leading to photoreceptor cell death. Additionally EAAT5 is connected to neurodegenerative diseases such as glaucoma where its dysfunction may affect visual processing and lead to progressive vision loss. In these contexts changes in the expression or activity of EAAT5 and its interaction with other transporters like EAAT1 can exacerbate disease progression by disrupting normal glutamatergic signaling.