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SLC6A17 is a neuronal, sodium-dependent, neutral amino acid transporter in the SLC6 family, mainly localized to synaptic vesicles in glutamatergic and some GABAergic neurons[1][3][4][5]. It selectively transports neutral amino acids such as glutamine, proline, leucine, alanine, and possibly glycine. Recent studies have defined glutamine as its endogenous substrate critical for synaptic vesicle function and possibly neurotransmission[2]. SLC6A17 activity is sodium-coupled and chloride-independent. Mutations in SLC6A17 cause autosomal recessive intellectual disability in humans, with mouse models showing defective learning and memory due to altered synaptic glutamine metabolism[2][5]. No clinically approved small molecule modulators exist, and its pharmacological targeting is largely unexplored.
Not applicable due to lack of known drugs; physiologically, the transporter catalyzes sodium-dependent uptake of neutral amino acids into vesicles, notably glutamine
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