Affinage

SLC38A1

Sodium-coupled neutral amino acid symporter 1 · UniProt Q9H2H9

Length
487 aa
Mass
54.0 kDa
Annotated
2026-06-10
53 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC38A1 (SNAT1/ATA1) is a Na+-coupled system A neutral amino acid transporter that supplies glutamine, alanine, and the system A-specific analog MeAIB with 1:1 Na+:amino acid stoichiometry and submillimolar affinity for glutamine, operating via an electrogenic, simultaneous transport mechanism in which Na+ binding precedes substrate (PMID:10891391, PMID:12684517). Transport activity requires N-glycosylation at N251/N257/N310, which is dispensable for plasma membrane trafficking (PMID:27655909). In the CNS, SNAT1 localizes to neuronal somata and proximal dendrites rather than nerve terminals or astrocytes (PMID:12684517), where it provides glutamine for GABA neurotransmitter synthesis: genetic disruption reduces vesicular GABA content, alters GABAergic synaptic vesicle morphology, and impairs critical-period cortical plasticity (PMID:31050701). The transporter is a hub for cellular amino acid economy beyond neurotransmission, mediating cysteine uptake to support glutathione synthesis under oxidative stress (PMID:20602128) and citrulline transport that sustains eNOS coupling and NO production (PMID:24454923). In cancer cells SLC38A1 drives glutaminolysis and growth through Akt/mTOR signaling (PMID:27129276, PMID:23848995, PMID:29108276), and its expression is controlled at multiple regulatory layers — by MeCP2-mediated transcriptional repression in microglia, where its derepression causes glutamine-dependent mitochondrial dysfunction and NMDA-receptor-dependent neurotoxicity (PMID:25673846), by CENPA-driven transcription (PMID:38382691), by METTL3/IGF2BP3 m6A-dependent mRNA stabilization (PMID:38701556), by OTUD5-mediated deubiquitination that protects it from proteasomal degradation (PMID:38658981), and by DSCR3-mediated endosomal recycling that maintains its surface abundance (PMID:35187626). In Th1 cells SLC38A1 is required for mTORC1 signaling, hexosamine biosynthesis, and tissue-specific autoimmune inflammation (PMID:41875885). In ischemic neurons it acts upstream of mTORC1-autophagy-dependent cell death (PMID:31552299).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2000 High

    Establishing the molecular identity of system A activity: the cloned human ATA1/SLC38A1 was shown to be a Na+-coupled neutral amino acid transporter, defining the gene's core biochemical function.

    Evidence Heterologous expression with radiotracer uptake and Na+-activation kinetics

    PMID:10891391

    Open questions at the time
    • Stoichiometry mechanism and full substrate range not yet resolved
    • No structural model of the transporter
  2. 2003 High

    Defining substrate selectivity, transport mechanism, and where in the CNS the transporter acts: SNAT1 was shown to be an electrogenic glutamine/alanine/MeAIB transporter in neuronal somata and dendrites, framing it as a supplier of glutamine to neurons.

    Evidence Radiotracer flux and electrophysiology in Xenopus oocytes plus confocal immunofluorescence

    PMID:12684517

    Open questions at the time
    • Functional consequence of neuronal localization for neurotransmission not yet tested
    • Mechanism linking transport to downstream metabolism unaddressed
  3. 2001 Medium

    Showing the transporter is dynamically regulated: cAMP signaling upregulates SLC38A1 transcription and transport, establishing inducible control of system A capacity.

    Evidence cAMP agonists with mRNA and MeAIB uptake assays plus transcription/translation inhibitors in HepG2

    PMID:11566196

    Open questions at the time
    • Transcription factor mediating the cAMP response not identified
    • Promoter elements undefined
  4. 2010 Medium

    Quantifying the physiological transport contribution and broadening substrate scope: SNAT1 accounts for most placental system A activity and can mediate cysteine uptake supporting glutathione synthesis under oxidative stress.

    Evidence siRNA knockdown with MeAIB kinetics in cytotrophoblasts; H2O2 stress with cysteine uptake and glutathione assays in cardiomyocytes

    PMID:20599747 PMID:20602128

    Open questions at the time
    • Stress-induced upregulation mechanism not defined
    • Tissue-specific regulation of substrate preference unclear
  5. 2011 Medium

    Resolving vascular localization: SNAT1 was found on larger cortical microvessels but excluded from BBB capillaries, distinguishing system A from system N transport at the brain vasculature.

    Evidence In vivo luminal biotinylation and immunofluorescence in mouse brain

    PMID:21364602

    Open questions at the time
    • Functional role at cortical microvessels not tested
    • Directionality of transport in vivo unknown
  6. 2014 Medium

    Linking transport to signaling output: SNAT1-mediated citrulline uptake was shown to sustain eNOS coupling and NO production, extending its role beyond glutamine supply.

    Evidence siRNA knockdown with NO and eNOS dimer/monomer assays in pulmonary endothelial cells under normoxia/hypoxia

    PMID:24454923

    Open questions at the time
    • Kinetics of citrulline transport not characterized
    • In vivo relevance to vascular NO signaling untested
  7. 2016 High

    Establishing SLC38A1 as a redundant but inducible glutamine route in cancer and identifying neurotoxic consequences of dysregulation: SNAT1 substitutes for ASCT2 to sustain glutamine uptake, while in microglia MeCP2 represses it to prevent glutamine-driven mitochondrial dysfunction and neurotoxicity.

    Evidence ASCT2 CRISPR knockout with SNAT1 siRNA, GCN2 silencing and growth assays; MeCP2 KO with SNAT1 overexpression, mitochondrial/ROS assays and antioxidant rescue

    PMID:25673846 PMID:27129276

    Open questions at the time
    • How MeCP2 represses the SLC38A1 promoter mechanistically not detailed
    • Whether transport per se or signaling drives microglial mitochondrial defects unresolved
  8. 2019 High

    Defining the in vivo neuronal function: genetic deletion of Slc38a1 impairs GABA synthesis, vesicular GABA loading, and cortical plasticity, and promotes mTORC1-autophagy-dependent neuronal death in ischemia.

    Evidence Slc38a1 KO and conditional (Synapsin-Cre) mice with GABA biochemistry, EM, electrophysiology, MCAO model and mTORC1/autophagy pharmacology

    PMID:31050701 PMID:31552299

    Open questions at the time
    • Direct biochemical link between SNAT1 and mTORC1 activation not established
    • Whether glutamine flux alone explains both GABA synthesis and ischemic death effects unclear
  9. 2017 Medium

    Building the cancer signaling picture: SLC38A1 knockdown reduces Akt/mTOR signaling, proliferation, migration, and tumor growth across breast and osteosarcoma models, placing it upstream of growth signaling.

    Evidence shRNA knockdown with signaling Westerns, proliferation/apoptosis assays and xenografts

    PMID:23848995 PMID:29108276

    Open questions at the time
    • No direct biochemical mechanism connecting transport to Akt/mTOR
    • Correlative signaling readouts without epistasis
  10. 2024 Medium

    Uncovering multilayered post-transcriptional and post-translational control: SLC38A1 is stabilized by OTUD5 deubiquitination, transcriptionally activated by CENPA, mRNA-stabilized by METTL3/IGF2BP3 m6A, and surface-maintained by DSCR3 recycling, each enhancing glutamine-fueled tumor growth.

    Evidence Co-IP/MS (OTUD5, DSCR3), promoter/reporter (CENPA), RIP and mRNA stability (METTL3/IGF2BP3) with glutamine uptake, proteasome assays and xenograft/orthotopic models

    PMID:35187626 PMID:38382691 PMID:38658981 PMID:38701556

    Open questions at the time
    • Whether these regulators act in the same tumors or distinct contexts unknown
    • Reciprocal validation of physical interactions limited to single labs
  11. 2023 High

    Defining a context-specific immunometabolic requirement: SLC38A1 is required in Th1 cells for mTORC1 signaling, hexosamine biosynthesis, and tissue-specific autoimmune inflammation, linking the transporter to adaptive immunity.

    Evidence In vivo CRISPR screen, conditional deletion, metabolomics, glycolysis assays and EAE/IBD/lung models

    PMID:41875885

    Open questions at the time
    • Basis of tissue-specific dependence (CNS vs lung) not mechanistically resolved
    • Whether glutamine supply alone accounts for the hexosamine and redox effects unclear
  12. 2026 Medium

    Proposing a non-canonical transceptor mode: in melanoma SNAT1 senses extracellular glutamine and signals via a P62/cMYC axis rather than mediating bulk influx, and in lung epithelium it scaffolds CMA-mediated DMT1 degradation to suppress ferroptosis.

    Evidence siPool knockdown with glutamine measurement, Co-IP and AlphaFold3 modeling (P62), Seahorse flux; AAV/lentiviral overexpression with Co-IP of DMT1/HSP90/HSC70/Lamp-2a complex in ALI models

    PMID:41483240 PMID:41976291

    Open questions at the time
    • Transceptor signaling mechanism distinct from transport not biochemically defined
    • Structural basis of the proposed P62 and chaperone complex interactions unconfirmed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SLC38A1 transport activity is mechanistically coupled to mTORC1/Akt signaling, and whether its transceptor signaling role is general or melanoma-specific, remains unresolved.
  • No structure of the human transporter
  • No direct biochemical link between substrate flux and downstream kinase activation
  • Transporter vs transceptor contributions not separated genetically

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0140104 molecular carrier activity 3
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1430728 Metabolism 3 R-HSA-382551 Transport of small molecules 3 R-HSA-112316 Neuronal System 2
Partners
DSCR3OTUD5SQSTM1

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Human ATA1/SLC38A1 encodes a 487-amino acid protein with 11 putative transmembrane domains that mediates Na+-coupled transport of neutral amino acids (system A-specific substrate α-methylaminoisobutyric acid) with 1:1 Na+:amino acid stoichiometry and Km of ~0.89 mM; the gene maps to human chromosome 12. Heterologous expression in mammalian cells, radiotracer uptake assays, Na+-activation kinetics Biochemical and biophysical research communications High 10891391
2003 SNAT1 mediates electrogenic, Na+-driven transport of glutamine (K0.5 ~0.3 mM), alanine, and MeAIB with 1:1 Na+:amino acid stoichiometry; Na+ binding precedes amino acid in a simultaneous mechanism; Li+ substitutes for Na+ but reduces Vmax; the transporter generates Na+-dependent presteady-state currents and a nonsaturable cation leak. SNAT1 protein localizes to somata and proximal dendrites of glutamatergic and GABAergic neurons throughout adult CNS but is absent from nerve terminals and astrocytes; luminal ependymal expression also detected. Radiotracer uptake and electrophysiology (current/flux) in Xenopus oocytes; confocal laser-scanning immunofluorescence; mutagenesis/kinetic analysis The Journal of biological chemistry High 12684517
2001 cAMP elevation (forskolin, cholera toxin, dibutyryl-cAMP) increases steady-state ATA1 (SLC38A1) mRNA levels and system A transport activity (increased Vmax, unchanged Km) in HepG2 cells; effect is blocked by protein kinase inhibitor H7, cycloheximide, and actinomycin D, indicating transcription- and translation-dependent upregulation. Northern blot/RT-PCR for mRNA levels; radiotracer MeAIB uptake assay; pharmacological inhibitors FEBS letters Medium 11566196
2010 SNAT1 contributes the majority (~75%) of system A amino acid transport activity in term human placental cytotrophoblast cells, as demonstrated by siRNA knockdown of SNAT1 significantly reducing MeAIB uptake; kinetic analysis resolved two transport systems consistent with SNAT1/SNAT2 (Km ~0.38 mM) and SNAT4 (Km ~45 mM). siRNA knockdown, 14C-MeAIB radiotracer uptake, kinetic (Michaelis-Menten) analysis Biochemical and biophysical research communications Medium 20599747
2010 Oxidative stress (H2O2) selectively upregulates SNAT1 protein expression in rat cardiomyocytes and enhances system A-mediated (αMeAIB-inhibitable) cysteine uptake; cysteine supplied via SNAT1 contributes to glutathione synthesis under oxidative conditions. qRT-PCR, Western blot, 35S-cysteine radiotracer uptake with oil filtration, glutathione enzymatic assay Amino acids Medium 20602128
2011 SNAT1 (Snat1) localizes to luminal membranes of larger cortical microvessels in mouse brain but is absent from BBB capillaries (where Snat3 is expressed), as shown by in vivo biotinylation and immunofluorescence colocalization, indicating distinct vascular roles for system A vs. system N transporters. In vivo luminal membrane biotinylation, immunofluorescence colocalization with cellular markers Journal of cerebral blood flow and metabolism Medium 21364602
2015 MeCP2 acts as a microglia-specific transcriptional repressor of SNAT1/SLC38A1. In MeCP2-deficient microglia, SNAT1 overexpression causes glutamine-dependent mitochondrial dysfunction (proliferating mitochondria, increased ROS, increased O2 consumption but decreased ATP), and overproduction of glutamate leading to NMDA receptor-dependent neurotoxicity. These defects are rescued by mitochondria-targeted catalase or SS-31 antioxidant peptide. MeCP2 knockdown/KO mouse model, SNAT1 overexpression in microglia, mitochondrial functional assays (OCR, ATP), ROS measurement, neurotoxicity assay, mitochondria-targeted antioxidant rescue The Journal of neuroscience High 25673846
2016 Net glutamine uptake in HeLa and 143B cancer cells does not depend on ASCT2 (SLC1A5) but requires SNAT1 (SLC38A1) and SNAT2 (SLC38A2). ASCT2 deletion does not reduce cell growth but triggers an amino acid starvation response (GCN2 activation) and upregulates SNAT1 to replace ASCT2 functionally; combined GCN2 silencing in ASCT2−/− background reduces cancer cell growth. CRISPR/Cas9 knockout of ASCT2, siRNA knockdown of SNAT1/SNAT2, amino acid uptake assays, GCN2 silencing, cell growth assays The Journal of biological chemistry High 27129276
2016 SNAT1 is an N-glycoprotein with three glycosylation sites at asparagine residues 251, 257, and 310 (N251 and N257 are primary sites). N-glycosylation-impaired mutants traffic normally to the cell surface but show significantly reduced glutamine (L-Gln) and MeAIB transport, indicating N-glycosylation is required for transport activity but not plasma membrane localization. N-glycosylation site mutagenesis, cell surface biotinylation, confocal immunofluorescence, 3H-MeAIB transport assay The Biochemical journal High 27655909
2019 Genetic disruption of Slc38a1 in mice impairs GABA synthesis, alters synaptic vesicle morphology in GABAergic presynapses, reduces vesicular GABA content, impairs critical period cortical plasticity, and affects high-frequency membrane oscillations and cortical processing. Slc38a1 knockout mice, GABA synthesis/content assays, electron microscopy of synaptic vesicles, electrophysiology, cortical plasticity assays Cerebral cortex High 31050701
2019 Neuron-specific deletion of Slc38a1 (using Synapsin I-Cre) reduces infarct size in mouse MCAO stroke model. SNAT1 promotes ischemic neuronal death via mTORC1 (p70S6K1 phosphorylation) activation; autophagy inhibitors abolish the neuroprotective effect of SNAT1 deficiency in vitro, placing SNAT1 upstream of mTORC1-autophagy-dependent neuronal death. Conditional Slc38a1 KO mice, MCAO model (TTC staining, MAP2-negative area), mTORC1 phosphorylation assays, rapamycin treatment, autophagy inhibitors, in vitro stroke culture Communications biology High 31552299
2013 Suppression of SNAT1 in breast cancer cells lowers phospho-Akt levels and inhibits cell growth, cell cycle progression, and induces apoptosis, linking SNAT1 activity to Akt signaling in cancer cells. shRNA knockdown of SNAT1, Western blot for p-Akt, cell viability, cell cycle, apoptosis assays BMC cancer Medium 23848995
2017 Silencing SNAT1 in osteosarcoma cells reduces proliferation, colony formation, and migration in vitro and tumor growth in xenograft models, and decreases expression of MMP9, vimentin, fibronectin, p-Akt, p-mTOR, and VEGF, suggesting SNAT1 acts upstream of Akt/mTOR signaling in osteosarcoma. shRNA knockdown, xenograft mouse model, Western blot for signaling proteins, proliferation and migration assays Oncotarget Medium 29108276
2023 SLC38A1 modulates hepatocellular carcinoma cell growth and migration via PI3K/AKT/mTOR signaling through glutamine-mediated energy metabolism; SLC38A1 knockdown suppresses this pathway. siRNA knockdown, Western blot for PI3K/AKT/mTOR pathway components, cell proliferation and migration assays Journal of cancer research and clinical oncology Low 37673823
2024 OTUD5 deubiquitinase directly binds SLC38A1 (confirmed by Co-IP and mass spectrometry) and prevents its ubiquitin-mediated proteasomal degradation, thereby stabilizing SLC38A1 protein levels. OTUD5 knockdown reduces SLC38A1 protein but not mRNA; SLC38A1 silencing attenuates OTUD5-driven HCC cell proliferation. Mass spectrometry, co-immunoprecipitation, OTUD5 overexpression/knockdown, proteasome inhibitor treatment, Western blot, xenograft mouse model Biology direct Medium 38658981
2024 CENPA directly regulates transcriptional activity of SLC38A1, increasing glutamine uptake and metabolism to promote endometrial cancer progression; CENPA overexpression/silencing reciprocally modulates SLC38A1 expression and glutamine metabolism. ChIP or luciferase transcriptional reporter assay (CENPA binding to SLC38A1 promoter), CENPA overexpression/knockdown, glutamine uptake measurement, tumor xenograft assay Cellular signalling Medium 38382691
2024 METTL3-mediated m6A methylation of the SLC38A1 3'UTR enhances SLC38A1 mRNA stability through IGF2BP3 recruitment; METTL3 silencing reduces intracellular glutamine content and inhibits cervical cancer cell viability, which is reversed by SLC38A1 overexpression. RNA immunoprecipitation (RIP) for METTL3/IGF2BP3 on SLC38A1 3'UTR, mRNA stability assay, METTL3/SLC38A1 overexpression/knockdown, glutamine content assay, tumor xenograft Biochemical and biophysical research communications Medium 38701556
2022 DSCR3 directly binds internalized SLC38A1 and mediates its sorting into a recycling pathway back to the plasma membrane, maintaining surface SLC38A1 abundance and enhancing glutamine uptake in MGMT-deficient glioblastoma cells; DSCR3 or SLC38A1 silencing increases temozolomide sensitivity. Label-free quantitative proteomics (plasma membrane fraction), co-immunoprecipitation, immunofluorescence of recycling, siRNA knockdown, in vitro and orthotopic brain tumor model Journal of neuro-oncology Medium 35187626
2014 SNAT1 mediates L-citrulline transport into pulmonary arterial endothelial cells; SNAT1 siRNA knockdown reduces basal NO production and prevents L-citrulline-induced increases in NO production and eNOS dimer-to-monomer ratios in both normoxic and hypoxic conditions, establishing that SNAT1-mediated citrulline transport regulates eNOS coupling and NO signaling. siRNA knockdown of SNAT1, NO production assay, eNOS dimer-to-monomer ratio (Western blot under non-reducing conditions), normoxia/hypoxia culture PloS one Medium 24454923
2017 Slc38a1 expression in brown adipose tissue is upregulated in obese mice in vivo and is induced in brown adipocytes by hypoxic stress through hypoxia-inducible factor-1α (HIF-1α), identifying HIF-1α as a transcriptional regulator of Slc38a1. In vivo obesity models (genetic and diet-induced), hypoxia treatment in brown adipocytes, HIF-1α manipulation, qRT-PCR and Western blot Pharmacology Low 29065407
2023 HPV16 E6 and E7 oncoproteins increase SNAT1 protein levels and stimulate glutaminolysis; cell proliferation in the presence of glutamine is partially dependent on SNAT1, as SNAT1 knockdown reduces proliferation and E6/E7-driven glutamine-dependent growth. HPV E6/E7 expression, E6/E7 siRNA knockdown, SNAT1 siRNA knockdown, glutamine dependence assay, cell proliferation assay Viruses Low 36851539
2023 SLC38A1 deficiency in Th1 cells (via CRISPR) reduces mTORC1 signaling and glycolytic activity, in part by reducing intracellular glutamine and disrupting hexosamine biosynthesis and redox regulation; SLC38A1 is required for Th1- but not Th17-driven autoimmune neuroinflammation (EAE) in a tissue-specific manner, while dispensable for lung inflammation. In vivo CRISPR screen, conditional genetic deletion, mTORC1 phosphorylation assay, metabolomics (glutamine, hexosamine pathway), glycolysis assay, EAE model, IBD model Cell metabolism High 41875885
2026 In melanoma cells, SNAT1 does not primarily mediate glutamine influx but instead signals in response to extracellular glutamine levels. SNAT1 interacts with P62 (SQSTM1) (confirmed by Co-IP and AlphaFold3 in silico modeling) and activates P62/cMYC signaling axis to regulate melanoma cell metabolism depending on glutamine availability, suggesting SNAT1 acts as a glutamine 'transceptor' rather than solely a transporter. siPool-mediated SNAT1 knockdown, intracellular/extracellular glutamine measurement, Co-IP, AlphaFold3 in silico protein interaction modeling, qRT-PCR and Western blot, Seahorse flux analysis, flow cytometry for mitochondria Cancers Medium 41976291
2026 SLC38A1 overexpression in alveolar type II epithelial cells promotes chaperone-mediated autophagy (CMA) degradation of divalent metal transporter 1 (DMT1) by facilitating interactions among DMT1, HSP90, HSC70, and Lamp-2a, enhancing lysosomal translocation of DMT1. This reduces intracellular iron and inhibits ferroptosis in acute lung injury. AAV6-mediated SLC38A1 overexpression in vivo (mouse LPS-ALI model), lentiviral overexpression in primary ATII cells, co-immunoprecipitation for DMT1/HSP90/HSC70/Lamp-2a complex, Western blot, TUNEL staining, shRNA knockdowns (SLC38A1, ULK1, HSP90) Inflammation Medium 41483240
2016 miR-593-3p targets Slc38a1 (and CLIP3) to negatively regulate insulin-promoted glucose consumption in HepG2 cells; insulin downregulates miR-593-3p, leading to increased Slc38a1 expression and enhanced glucose metabolism. miR-593-3p overexpression/inhibition, 3'UTR luciferase reporter assay for Slc38a1, glucose consumption assay, insulin treatment, Western blot and qRT-PCR Journal of molecular endocrinology Low 27613819

Source papers

Stage 0 corpus · 53 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 Deletion of Amino Acid Transporter ASCT2 (SLC1A5) Reveals an Essential Role for Transporters SNAT1 (SLC38A1) and SNAT2 (SLC38A2) to Sustain Glutaminolysis in Cancer Cells. The Journal of biological chemistry 211 27129276
2020 lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis. Aging 152 32453709
2003 Functional properties and cellular distribution of the system A glutamine transporter SNAT1 support specialized roles in central neurons. The Journal of biological chemistry 126 12684517
2000 Cloning and functional expression of ATA1, a subtype of amino acid transporter A, from human placenta. Biochemical and biophysical research communications 93 10891391
2015 Dysregulation of glutamine transporter SNAT1 in Rett syndrome microglia: a mechanism for mitochondrial dysfunction and neurotoxicity. The Journal of neuroscience : the official journal of the Society for Neuroscience 77 25673846
2013 Activation of SNAT1/SLC38A1 in human breast cancer: correlation with p-Akt overexpression. BMC cancer 58 23848995
2007 Activation of a system A amino acid transporter, ATA1/SLC38A1, in human hepatocellular carcinoma and preneoplastic liver tissues. International journal of oncology 54 17549407
2010 The contribution of SNAT1 to system A amino acid transporter activity in human placental trophoblast. Biochemical and biophysical research communications 45 20599747
2019 The Glutamine Transporter Slc38a1 Regulates GABAergic Neurotransmission and Synaptic Plasticity. Cerebral cortex (New York, N.Y. : 1991) 38 31050701
2019 Inhibition of the glutamine transporter SNAT1 confers neuroprotection in mice by modulating the mTOR-autophagy system. Communications biology 36 31552299
2017 SLC38A1 promotes proliferation and migration of human colorectal cancer cells. Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban 32 28224429
2022 Role of Amino Acid Transporter SNAT1/SLC38A1 in Human Melanoma. Cancers 30 35565278
2011 Differential axial localization along the mouse brain vascular tree of luminal sodium-dependent glutamine transporters Snat1 and Snat3. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 30 21364602
2022 Long non-coding RNA OGFRP1 regulates cell proliferation and ferroptosis by miR-299-3p/SLC38A1 axis in lung cancer. Anti-cancer drugs 28 36066402
2021 CircRUNX1 functions as an oncogene in colorectal cancer by regulating circRUNX1/miR-485-5p/SLC38A1 axis. European journal of clinical investigation 28 33769559
2001 Differential influence of cAMP on the expression of the three subtypes (ATA1, ATA2, and ATA3) of the amino acid transport system A. FEBS letters 28 11566196
2010 Overexpression of ATA1/SLC38A1 predicts future recurrence and death in Chinese patients with hilar cholangiocarcinoma. The Journal of surgical research 26 20605601
2003 Ontogeny of the neutral amino acid transporter SAT1/ATA1 in rat brain. Brain research. Developmental brain research 26 12855186
2012 Promotion of both proliferation and neuronal differentiation in pluripotent P19 cells with stable overexpression of the glutamine transporter slc38a1. PloS one 24 23110224
2024 OTUD5 promotes the growth of hepatocellular carcinoma by deubiquitinating and stabilizing SLC38A1. Biology direct 22 38658981
2010 Oxidative stress increases SNAT1 expression and stimulates cysteine uptake in freshly isolated rat cardiomyocytes. Amino acids 21 20602128
2023 Integrative analysis reveals that SLC38A1 promotes hepatocellular carcinoma development via PI3K/AKT/mTOR signaling via glutamine mediated energy metabolism. Journal of cancer research and clinical oncology 19 37673823
2024 CENPA promotes glutamine metabolism and tumor progression by up-regulating SLC38A1 in endometrial cancer. Cellular signalling 18 38382691
2011 Exacerbated vulnerability to oxidative stress in astrocytic C6 glioma cells with stable overexpression of the glutamine transporter slc38a1. Neurochemistry international 18 21219957
2014 Sodium-coupled neutral amino acid transporter 1 (SNAT1) modulates L-citrulline transport and nitric oxide (NO) signaling in piglet pulmonary arterial endothelial cells. PloS one 16 24454923
2013 shRNA-mediated Slc38a1 silencing inhibits migration, but not invasiveness of human pancreatic cancer cells. Chinese journal of cancer research = Chung-kuo yen cheng yen chiu 15 24255574
2022 Hsa_circ_0003602 Contributes to the Progression of Colorectal Cancer by Mediating the miR-149-5p/SLC38A1 Axis. Gut and liver 14 36148577
2017 Increased SNAT1 is a marker of human osteosarcoma and potential therapeutic target. Oncotarget 14 29108276
2021 Functional Characterization of Serotonin N-Acetyltransferase Genes (SNAT1/2) in Melatonin Biosynthesis of Hypericum perforatum. Frontiers in plant science 12 34950170
2023 HPV16 E6 and E7 Oncoproteins Stimulate the Glutamine Pathway Maintaining Cell Proliferation in a SNAT1-Dependent Fashion. Viruses 10 36851539
2020 Long Noncoding RNA NEAT1 Contributes to the Tumorigenesis of Colorectal Cancer Through Regulating SLC38A1 Expression by Sponging miR-138. Cancer biotherapy & radiopharmaceuticals 10 32700988
2016 MicroRNA-593-3p regulates insulin-promoted glucose consumption by targeting Slc38a1 and CLIP3. Journal of molecular endocrinology 10 27613819
2015 Upregulation of Slc38a1 Gene Along with Promotion of Neurosphere Growth and Subsequent Neuronal Specification in Undifferentiated Neural Progenitor Cells Exposed to Theanine. Neurochemical research 10 25957749
2023 Tissue-Specific Dependence of Th1 Cells on the Amino Acid Transporter SLC38A1 in Inflammation. bioRxiv : the preprint server for biology 9 37745344
2020 Selective Upregulation by Theanine of Slc38a1 Expression in Neural Stem Cell for Brain Wellness. Molecules (Basel, Switzerland) 9 31952134
2009 SNAT1 and a family with high rates of suicidal behavior. Neuroscience 9 19442705
2024 METTL3-mediated m6A methylation of SLC38A1 stimulates cervical cancer growth. Biochemical and biophysical research communications 7 38701556
2022 Recycling of SLC38A1 to the plasma membrane by DSCR3 promotes acquired temozolomide resistance in glioblastoma. Journal of neuro-oncology 7 35187626
2022 miRNA-432 and SLC38A1 as Predictors of Hepatocellular Carcinoma Complicated with Alcoholic Steatohepatitis. Oxidative medicine and cellular longevity 7 35663198
2017 Hypoxic Stress Upregulates the Expression of Slc38a1 in Brown Adipocytes via Hypoxia-Inducible Factor-1α. Pharmacology 7 29065407
2005 Ontogeny of the neutral amino acid transporter SNAT1 in the developing rat. Journal of molecular histology 7 16200463
2024 Investigation of Roles of SLC38A1 in Proliferation and Differentiation of Mouse Tongue Epithelium and Expression in Human Oral Tongue Squamous Cell Carcinoma. Cancers 5 38254895
2024 Clock protein LHY targets SNAT1 and negatively regulates the biosynthesis of melatonin in Hypericum perforatum. Science advances 4 39292789
2025 GluOC Induced SLC7A11 and SLC38A1 to Activate Redox Processes and Resist Ferroptosis in TNBC. Cancers 3 40075587
2024 circTADA2A inhibited SLC38A1 expression and suppresses melanoma progression through the prevention of CNBP trans-activation. PloS one 3 38635778
2026 Manipulation of the Expression of SNAT1 Enhances Melatonin Biosynthesis, Promotes Plant Growth, and Improves Salt Stress Tolerance in Kiwifruit. Journal of pineal research 2 41503875
2026 SLC38A1 Inhibits Ferroptosis of Alveolar Type II Epithelial Cells in Acute Lung Injury by Promoting Autophagic Degradation of Divalent Metal Transporter 1 (DMT1): an In Vivo and In Vitro Study. Inflammation 1 41483240
2025 Complement C5a promotes human retinal pigment epithelial cell viability and migration through SLC38A1-mediated glutamine metabolism. Medical microbiology and immunology 1 40358757
2025 Structural and Functional Features of Melatonin Biosynthesis Genes SNAT1 and SNAT2 in Tomato and Garlic Plants. Doklady. Biochemistry and biophysics 1 41329272
2022 miR-373-3p Regulates the Proliferative and Migratory Properties of Human HTR8 Cells via SLC38A1 Modulation. Disease markers 1 35837487
2016 N-Glycosylation influences transport, but not cellular trafficking, of a neuronal amino acid transporter SNAT1. The Biochemical journal 1 27655909
2026 Tissue and CD4 T cell subset dependence on the amino acid transporter SLC38A1. Cell metabolism 0 41875885
2026 SNAT1 (SLC38A1) Is Not the Main Glutamine Transporter in Melanoma, but Controls Metabolism via Glutamine-Dependent Activation of P62 (SQSTM1)/cMYC-Axis. Cancers 0 41976291

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