Target intelligence / Profile preview

Sodium-coupled neutral amino acid transporter 7 (SLC38A7)

Target
SLC38A7
Molecular classification
Transporter, Solute carrier (SLC) family protein, Symporter, Membrane protein
01

Overview

Sodium-coupled neutral amino acid transporter 7 (SLC38A7, also known as SNAT7) is a **lysosomal membrane transporter** belonging to the solute carrier (SLC) family of proteins. It mediates the sodium-dependent export of **L-glutamine and L-asparagine from the lysosome into the cytosol** following lysosomal protein degradation[1][3][4][5]. SNAT7 is highly specific to these amino acids and is activated under acidic lysosomal pH, unlike other broadly-selective SLC38 family members[1]. SNAT7 is crucial for nutrient supply and growth in cancer cells facing glutamine scarcity, where it enables utilization of extracellular proteins internalized via macropinocytosis and processed by lysosomes[1][4][6]. It has also been identified as a regulator of mTORC1, a central pathway in cell growth and metabolism, particularly upon uptake of extracellular proteins[6]. In the brain, SLC38A7 is expressed in neurons and likely participates in neurotransmitter recycling, further contributing to CNS amino acid metabolism[2]. SLC38A7 does not have approved drugs directly targeting it but is under investigation as a candidate for anti-cancer strategies aimed at disrupting amino acid supply in nutrient-scavenging tumors[1][6]. Its essential role in normal physiological processes, including possible neuronal function, presents therapeutic challenges regarding specificity and safety[1][2].

Other names
SLC38A7SNAT7FLJ10815Solute carrier family 38 member 7amino acid transportersodium-coupled neutral amino acid transporter 7putative sodium-coupled neutral amino acid transporter 7
02

Mechanism of action

Sodium-coupled symport of L-glutamine and L-asparagine from lysosome to cytoplasm, activation of mTORC1 pathway via nutrient sensing, supporting cell proliferation in glutamine-depleted environments

03

Biological functions

Lysosomal export of amino acids (especially glutamine and asparagine)Regulation of cellular amino acid homeostasismTORC1 activationSupport of cell growth under amino acid-limited conditionsNeurotransmitter cycling (neuronal glutamine/glutamate cycle)
04

Disease associations

Cancer (notably growth support in nutrient-poor tumors)Potential role in neurobiology (glutamate/glutamine recycling)Other (general amino acid metabolism disorders)
05

Safety considerations

Potential broad effects due to general role in amino acid homeostasisrisk of affecting normal neuronal and systemic amino acid handlingchallenges in tissue-specific targeting
06

Interacting drugs

None known as direct inhibitors/modulators as of current literature; experimental targeting considered for cancer metabolism
07

Biomarkers

Potential biomarker for nutrient-scavenging cancer cells (e.g., some pancreatic and other solid tumors dependent on lysosomal amino acid export)

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