Affinage

SLC6A15

Sodium-dependent neutral amino acid transporter B(0)AT2 · UniProt Q9H2J7

Length
730 aa
Mass
81.8 kDa
Annotated
2026-06-10
25 papers in source corpus 13 papers cited in narrative 15 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC6A15 (B0AT2/SBAT1) is a sodium-coupled plasma-membrane transporter of hydrophobic, zwitterionic amino acids that controls neuronal amino acid pools and feeds glutamate/glutamine metabolism, with downstream consequences for glutamatergic signaling and stress-related behavior (PMID:16226721, PMID:26228428). Heterologous expression established it as a Na+-dependent symporter with strong preference for branched-chain amino acids (leucine, isoleucine, valine) and methionine that excludes aromatic, charged, and beta-amino acids, while PKC activation reduces its surface population (PMID:16226721); genetic knockout confirmed it contributes to synaptosomal proline and leucine uptake in vivo (PMID:17931606). In the brain, SLC6A15 mediates the anorexigenic effect of leucine via the ventromedial hypothalamus (PMID:23505546, PMID:24023709). In the hippocampus, it sets intracellular proline and neutral amino acid levels and thereby tissue glutamate/glutamine, and bidirectionally controls extracellular glutamate tone, glutamatergic synapse release probability, and GluR1-dependent signaling in the dentate gyrus (PMID:26228428, PMID:26585320, PMID:33007132). Reduction of SLC6A15 in nucleus accumbens D2-medium spiny neurons specifically drives susceptibility to social defeat stress, and restoring its expression in these neurons prevents stress-induced social avoidance (PMID:28576941). The protein adopts a 12-transmembrane-domain topology with intracellular termini and glycosylated extracellular loops and traffics to the cell surface (PMID:11112352); selective small-molecule inhibitors of the transporter have been identified that stimulate neurite outgrowth.

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2000 Medium

    Defining the protein architecture and surface destination of SLC6A15 established it as a candidate plasma-membrane transporter rather than an intracellular protein.

    Evidence Epitope-tagged construct transfection with subcellular imaging and topology prediction

    PMID:11112352

    Open questions at the time
    • No substrate or transport activity demonstrated at this stage
    • Trafficking determinants and regulation of surface delivery not defined
  2. 2005 High

    Heterologous reconstitution answered what SLC6A15 actually transports, defining it as a Na+-coupled symporter selective for branched-chain amino acids, methionine, and imino acids and revealing PKC-dependent surface regulation.

    Evidence Xenopus oocyte expression with radiolabeled uptake, kinetics, and PKC manipulation

    PMID:16226721

    Open questions at the time
    • Stoichiometry of Na+ coupling not resolved
    • Molecular mechanism of PKC-driven surface loss (direct phosphorylation vs. trafficking) not established
  3. 2007 High

    Knockout synaptosome uptake confirmed the in vitro substrate profile reflects a genuine in vivo contribution to neuronal proline and leucine transport.

    Evidence Slc6a15 knockout mouse cortical synaptosome radiolabeled uptake

    PMID:17931606

    Open questions at the time
    • Residual uptake indicates redundancy with other transporters
    • Does not localize transport to specific synaptic compartments
  4. 2013 High

    Knockout phenotyping linked SLC6A15 transport function to a physiological output, showing it mediates leucine-induced hypothalamic neuronal activation and reduction of food intake.

    Evidence Slc6a15 KO mice with ICV leucine, c-Fos activation, feeding assays, and tissue distribution mapping

    PMID:23505546 PMID:24023709

    Open questions at the time
    • Sex-selective effects not mechanistically explained
    • Downstream signaling from leucine uptake to satiety circuitry unresolved
  5. 2015 High

    Bidirectional genetic manipulation established the central mechanistic role: SLC6A15 controls hippocampal neutral amino acid and glutamate/glutamine pools, extracellular glutamate tone, and stress/anxiety behavior via glutamatergic GluR1 signaling.

    Evidence Slc6a15 KO and viral overexpression with HPLC/NMR amino acid measurement, microdialysis, behavioral tests, and GluR1/GluR2/NR1 immunoblot

    PMID:26228428 PMID:26585320

    Open questions at the time
    • Causal chain from amino acid pool changes to GluR1 regulation not directly demonstrated
    • Cell type responsible for the hippocampal glutamate changes not pinpointed
  6. 2017 High

    Cell-type-specific manipulation pinpointed the circuit basis of stress behavior, showing SLC6A15 in NAc D2-medium spiny neurons bidirectionally gates social defeat stress susceptibility.

    Evidence Cre-inducible viral knockdown/restoration in D2-Cre and A2A-Cre mice with social defeat paradigms and protein localization

    PMID:28576941

    Open questions at the time
    • Transport substrate driving the D2-MSN phenotype not identified
    • Connection to the hippocampal glutamate mechanism not established
  7. 2020 Medium

    Cellular profiling of knockout neurons extended SLC6A15's role beyond glutamate to mitochondrial function, redox balance, and neurite outgrowth, broadening its metabolic footprint.

    Evidence Primary KO hippocampal neurons with proteomics, electrophysiology, Seahorse, GSH/GSSG, and neurite outgrowth assays

    PMID:33007132

    Open questions at the time
    • Mechanism linking amino acid transport to mitochondrial/redox changes unresolved
    • Single-lab cellular study without in vivo confirmation of metabolic effects
  8. 2025 Medium

    Loss-of-function in melanocytes uncovered a non-neuronal role, with SLC6A15-mediated phenylalanine transport driving UVB-responsive melanogenesis.

    Evidence siRNA/shRNA knockdown in MNT1 cells and primary melanocytes with pigmentation, tyrosinase, gene expression, amino acid, and UVB assays

    PMID:41352278

    Open questions at the time
    • Phenylalanine as a direct SLC6A15 substrate conflicts with the neuronal aromatic-amino-acid exclusion and needs reconciliation
    • Transcriptional link from amino acid levels to MITF not defined
  9. 2026 Medium

    Pharmacological tool development provided the first selective inhibitors of SLC6A15, validating it as a druggable target and reproducing the neurite outgrowth phenotype.

    Evidence High-throughput [3H]proline uptake screen in overexpressing HEK293 cells with SLC6 selectivity profiling and neurite outgrowth (preprint)

    Open questions at the time
    • In vivo efficacy and behavioral effects of inhibitors untested
    • Preprint, single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SLC6A15 transport activity is regulated post-translationally and how substrate uptake mechanistically couples to glutamate signaling and stress circuitry remain open.
  • pS701/pS699/pS687 sites and predicted kinases MAPK3/CDK12 not experimentally confirmed
  • Binary interactors (Lyn, EGFR, calnexin) lack direct validation
  • Structure of SLC6A15 and substrate-binding determinants not solved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 6 GO:0140104 molecular carrier activity 2
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-382551 Transport of small molecules 2

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 SLC6A15 (SBAT1) functions as a sodium-coupled transporter of hydrophobic, zwitterionic alpha-amino and imino acids when expressed in Xenopus oocytes, with strong preference for branched-chain amino acids (leucine, isoleucine, valine) and methionine (K0.5 80-160 µM); it excludes aromatic or charged amino acids, beta-amino acids, glycine, and GABA. Transport is highly temperature-dependent (Q10=9) and inhibited at acidic pH. PKC activation reduces the plasma-membrane population of SBAT1 protein. Xenopus oocyte heterologous expression, radiolabeled substrate uptake assays, pharmacological manipulation (PKC activation) Biochemical and biophysical research communications High 16226721
2007 In cortical synaptosomes from v7-3 (SLC6A15) knockout mice, sodium-dependent proline uptake was reduced by 15% and leucine uptake by 40% compared to wild-type controls, establishing SLC6A15 as a contributor to synaptosomal proline and leucine transport in vivo. SLC6A15 knockout mouse model; radiolabeled amino acid uptake into cortical synaptosomes Brain research High 17931606
2000 Human v7-3 (SLC6A15) encodes a 730 amino acid protein with 12 predicted transmembrane domains, intracellular N- and C-termini, and large extracellular loops between TM3-4 and TM7-8 with N-linked glycosylation sites; transfection experiments showed v7-3 is expressed at the cell surface (plasma membrane localization), in contrast to the related NTT5 which is predominantly intracellular. Epitope-tagged transporter construct transfection, subcellular localization by cellular imaging/fractionation; bioinformatic topology prediction Genomics Medium 11112352
2013 SLC6A15 knockout mice show lower reduction in food intake and lower neuronal activation in the ventromedial hypothalamic nucleus (VMH) in response to intracerebroventricular leucine injections compared to wild-type mice, establishing SLC6A15 as mediating the anorexigenic effect of leucine in the brain. B0AT2 (SLC6A15) immunoreactivity was found in neurons (including GABAergic neurons and spinal cord motor neurons) and in astrocytes near ventricles, and co-localized with cytokeratin and diazepam binding inhibitor (DBI) in choroid plexus epithelial cells. Slc6a15 knockout mice, food intake assay with leucine injection, c-Fos neuronal activation immunohistochemistry, immunohistochemistry and in situ hybridization for tissue distribution PloS one High 23505546
2013 SLC6A15 knockout attenuates leucine's ability to reduce normal chow intake and weight gain on high-fat diet in a sex-selective fashion in mice, supporting a role for brain SLC6A15 in leucine-mediated control of food intake and obesity-related phenotypes. Slc6a15 knockout mice, dietary feeding assays with leucine supplementation, body weight measurement PloS one Medium 24023709
2015 Loss of SLC6A15 in knockout mice reduces hippocampal tissue levels of proline and other neutral amino acids, decreases overall tissue glutamate and glutamine, while simultaneously increasing basal extracellular glutamate tone. Conversely, hippocampal SLC6A15 overexpression increases glutamate/glutamine tissue concentrations. These neurochemical changes were linked to altered sensorimotor gating behavior. Slc6a15 knockout mice; virus-mediated hippocampal overexpression; hippocampal amino acid measurement (HPLC/NMR); in vivo microdialysis for extracellular glutamate; prepulse inhibition behavioral test Journal of psychiatric research High 26228428
2015 Slc6a15 knockout mice show reduced anxiety- and depressive-like behavior following chronic social stress compared to wild-type littermates, while hippocampal SLC6A15 overexpression increases anxiety-like behavior at baseline. GluR1 (AMPA receptor subunit) expression in the dentate gyrus, but not GluR2 or NR1, is regulated by slc6a15 expression levels, implicating glutamatergic signaling as a downstream mechanism. Slc6a15 KO and virus-mediated hippocampal overexpression mouse models; chronic social stress paradigm; anxiety/depression behavioral tests; immunoblot for GluR1, GluR2, NR1 in dentate gyrus Stress (Amsterdam, Netherlands) Medium 26585320
2017 Cre-inducible viral reduction of Slc6a15 selectively in NAc D2-medium spiny neurons (using D2-Cre and A2A-Cre mice) causes enhanced susceptibility to subthreshold social defeat stress, while restoring Slc6a15 expression in D2-neurons after chronic social defeat stress prevents social avoidance. Slc6a15 protein was unaltered in ChAT interneurons after chronic social defeat stress, indicating the effect is D2-MSN-specific. Cre-inducible viral vectors in D2-Cre and A2A-Cre mice; chronic and subthreshold social defeat stress; social interaction behavioral testing; immunofluorescence for Slc6a15 protein in ChAT interneurons The Journal of neuroscience High 28576941
2013 Two rare non-synonymous coding variants in SLC6A15 were associated with significantly increased maximal [3H]proline uptake compared to the wildtype sequence in a cellular uptake assay, demonstrating that specific amino acid changes can alter transporter activity. Cellular [3H]proline uptake assay with wildtype vs. mutant SLC6A15 constructs; pooled targeted re-sequencing and individual re-genotyping PloS one Medium 23874702
2020 Loss of SLC6A15 in primary hippocampal neurons results in: reduced release probability at glutamatergic synapses, increased mitochondrial function, higher GSH/GSSG redox ratio, and improved neurite outgrowth. Proteomics of Slc6a15-KO hippocampal tissue revealed differentially regulated proteins in metabolic, mitochondrial, and structural functional domains. Primary hippocampal neurons from Slc6a15-KO mice; proteomics (mass spectrometry); electrophysiology (glutamatergic synapse release probability); Seahorse metabolic assay (mitochondrial function); GSH/GSSG redox assay; neurite outgrowth imaging The European journal of neuroscience Medium 33007132
2021 Ectopic overexpression of SLC6A15 in papillary thyroid cancer (PTC) cells impaired their migratory and invasive abilities in vitro, and intercellular adhesion molecule-1 (ICAM-1) was identified as involved in mediating these effects. SLC6A15 overexpression in PTC cell lines; Transwell migration and invasion assays; ICAM-1 expression analysis Journal of cellular biochemistry Low 33690923
2025 SLC6A15 knockdown in MNT1 cells and primary melanocytes reduced melanin synthesis, downregulated melanogenesis-related genes (MITF, TYR, DCT), decreased tyrosinase activity, and reduced intracellular phenylalanine levels. UVB exposure upregulated SLC6A15, and SLC6A15 silencing abrogated UVB-induced pigmentation, establishing SLC6A15-mediated phenylalanine transport as a mechanism regulating melanogenesis. SLC6A15 knockdown (siRNA/shRNA) in melanocyte cell lines and primary melanocytes; Fontana-Masson staining; tyrosinase activity assay; RT-qPCR for melanogenesis genes; intracellular amino acid measurement; UVB irradiation experiments Journal of photochemistry and photobiology. B, Biology Medium 41352278
2025 Ectopic overexpression of SLC6A15 in CD8+ T-cells was sufficient to restore effector function (cytotoxic capacity and protein synthesis) in tumor-infiltrating lymphocytes, demonstrating that SLC6A15-mediated amino acid transport can relieve amino acid insufficiency-driven translational suppression in the tumor microenvironment. SLC6A15 overexpression in primary CD8+ T-cells; tumor infiltrating lymphocyte functional assays; protein synthesis measurement; cytotoxicity assays bioRxivpreprint Low
2026 High-throughput screening of 200,000 compounds identified the first selective inhibitors of B0AT2/SLC6A15, with a 1,5-benzodiazepine series showing IC50 ~250 nM in [3H]proline uptake assays in SLC6A15-overexpressing HEK293 cells and primary neurons, no detectable inhibition of SERT, DAT, GAT1, or NTT4/SLC6A17 (>80 µM), and dose-dependent stimulation of neurite outgrowth in primary neurons. High-throughput [3H]proline cellular uptake assay in SLC6A15-overexpressing HEK293 cells; selectivity profiling against related SLC6 transporters; neurite outgrowth assay in primary hippocampal neurons bioRxivpreprint Medium
2026 Phosphoproteomic curation identified three predominant phosphorylation sites on SLC6A15: pS701, pS699, and pS687, with predicted upstream kinases MAPK3 and CDK12. Binary interactors identified include tyrosine-protein kinase Lyn, epidermal growth factor receptor, and calnexin. Computational curation and bioinformatic analysis of 3825 global phosphoproteomic datasets; kinase prediction; binary interactor analysis Omics : a journal of integrative biology Low 41649124

Source papers

Stage 0 corpus · 25 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 The neuronal transporter gene SLC6A15 confers risk to major depression. Neuron 168 21521612
2005 Characterization of a branched-chain amino-acid transporter SBAT1 (SLC6A15) that is expressed in human brain. Biochemical and biophysical research communications 72 16226721
2017 Reduced Slc6a15 in Nucleus Accumbens D2-Neurons Underlies Stress Susceptibility. The Journal of neuroscience : the official journal of the Society for Neuroscience 39 28576941
2000 Cloning and characterization of human NTT5 and v7-3: two orphan transporters of the Na+/Cl- -dependent neurotransmitter transporter gene family. Genomics 39 11112352
2012 A variant of the neuronal amino acid transporter SLC6A15 is associated with ACTH and cortisol responses and cognitive performance in unipolar depression. The international journal of neuropsychopharmacology 32 22475622
2013 Involvement of the neutral amino acid transporter SLC6A15 and leucine in obesity-related phenotypes. PloS one 25 24023709
2019 Edaravone presents antidepressant-like activity in corticosterone model of depression in mice with possible role of Fkbp5, Comt, Adora1 and Slc6a15 genes. Toxicology and applied pharmacology 22 31344373
2015 The amino acid transporter SLC6A15 is a regulator of hippocampal neurochemistry and behavior. Journal of psychiatric research 22 26228428
2013 B(0)AT2 (SLC6A15) is localized to neurons and astrocytes, and is involved in mediating the effect of leucine in the brain. PloS one 22 23505546
2015 SLC6A15, a novel stress vulnerability candidate, modulates anxiety and depressive-like behavior: involvement of the glutamatergic system. Stress (Amsterdam, Netherlands) 21 26585320
2007 Deletion of v7-3 (SLC6A15) transporter allows assessment of its roles in synaptosomal proline uptake, leucine uptake and behaviors. Brain research 20 17931606
2023 The SLC6A15-SLC6A20 Neutral Amino Acid Transporter Subfamily: Functions, Diseases, and Their Therapeutic Relevance. Pharmacological reviews 19 37940347
1996 Widespread brain distribution of mRNA encoding the orphan neurotransmitter transporter v7-3. Brain research. Molecular brain research 19 8738154
2016 Effects of a Polymorphism of the Neuronal Amino Acid Transporter SLC6A15 Gene on Structural Integrity of White Matter Tracts in Major Depressive Disorder. PloS one 18 27723767
2019 Fine-scale haplotype mapping of MUT, AACS, SLC6A15 and PRKCA genes indicates association with insulin resistance of metabolic syndrome and relationship with branched chain amino acid metabolism or regulation. PloS one 15 30913280
2013 Functional coding variants in SLC6A15, a possible risk gene for major depression. PloS one 12 23874702
2020 Loss of the psychiatric risk factor SLC6A15 is associated with increased metabolic functions in primary hippocampal neurons. The European journal of neuroscience 11 33007132
2018 Withdrawal of caffeine after its chronic administration modifies the antidepressant-like activity of atypical antidepressants in mice. Changes in cortical expression of Comt, Slc6a15 and Adora1 genes. Psychopharmacology 8 29882086
2021 SLC6A15 acts as a tumor suppressor to inhibit migration and invasion in human papillary thyroid cancer. Journal of cellular biochemistry 7 33690923
2012 A conserved threonine in the S1-S2 loop of KV7.2 and K V7.3 channels regulates voltage-dependent activation. Pflugers Archiv : European journal of physiology 7 23271449
2017 A Combined Study of SLC6A15 Gene Polymorphism and the Resting-State Functional Magnetic Resonance Imaging in First-Episode Drug-Naive Major Depressive Disorder. Genetic testing and molecular biomarkers 3 28915082
2026 Phosphorylation-Dependent Regulation and Interactions of the Neutral Amino Acid Transporter SLC6A15: Implications for Major Depression and Neuropsychiatric Disorders. Omics : a journal of integrative biology 0 41649124
2026 Unlocking SLC6A15 (B0AT2): A Dual-Platform Approach To Accelerate Drug Discovery for Neuropsychiatric Disorders. Analytical chemistry 0 42118683
2025 UVB enhances SLC6A15-mediated phenylalanine transport to promote melanogenesis. Journal of photochemistry and photobiology. B, Biology 0 41352278
2024 LncRNA DGUOK-AS1 Promotes Cell Progression in Lung Squamous Cell Carcinoma by Regulation of miR-653-5p/SLC6A15 Axis. Molecular biotechnology 0 38407689

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