Affinage

SLC6A19

Sodium-dependent neutral amino acid transporter B(0)AT1 · UniProt Q695T7

Length
634 aa
Mass
71.1 kDa
Annotated
2026-06-10
49 papers in source corpus 17 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC6A19 (B0AT1) is the principal apical, sodium-dependent, chloride-independent transporter that drives bulk reabsorption and absorption of neutral amino acids in renal proximal tubule and intestinal enterocytes, and its loss-of-function mutations cause Hartnup disorder (PMID:15286787, PMID:15286788). It mediates electrogenic Na+:amino acid co-transport with 1:1 stoichiometry through an ordered mechanism in which the amino acid binds before Na+, accepting all neutral amino acids with preference for large non-aromatic substrates (PMID:15804236, PMID:16133263). Catalytically competent surface expression requires tissue-specific ancillary partners — collectrin (TMEM27) in kidney and ACE2 in intestine — with collectrin contacting transmembrane faces that separately govern membrane delivery and catalytic activation (PMID:19472175, PMID:26240152). At the intestinal brush border B0AT1 assembles into functional digestive complexes with the peptidases aminopeptidase N and ACE2, where APN raises apparent substrate affinity and surface expression, and a single ACE2:B0AT1 heterodimer constitutes the minimal transport unit within a larger dimer-of-heterodimers assembly (PMID:22677001, PMID:34847569). Transport activity is acutely up-regulated by kinases SGK1-3, PKB/Akt (via PIKfyve), and JAK2, all increasing transporter abundance at the plasma membrane without changing affinity (PMID:20511718, PMID:21964291, PMID:23234856). Genetic ablation in mice abolishes epithelial neutral amino acid uptake and reduces body weight, postprandial insulin secretion, and intestinal mTOR signaling while activating the GCN2/ATF4 stress response, establishing the transporter as essential for systemic nutrient sensing (PMID:21636576). Hartnup-causing variants act through endoplasmic reticulum retention and failure to reach the plasma membrane, with some variants additionally disrupting ACE2 trafficking (PMID:40852587).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2004 High

    Established the molecular identity of the long-sought intestinal/renal neutral amino acid transporter and tied it directly to a human Mendelian disease.

    Evidence Positional cloning, mutation identification, and in vitro transport assays in heterologous systems

    PMID:15286787 PMID:15286788

    Open questions at the time
    • Transport mechanism and stoichiometry not yet resolved
    • Ancillary requirements for surface expression unknown
  2. 2005 High

    Defined the biophysical transport mechanism, answering how ion coupling and substrate order produce electrogenic uptake.

    Evidence Two-electrode voltage-clamp with simultaneous charge and radiolabeled amino acid flux in Xenopus oocytes; kinetic modeling

    PMID:15804236 PMID:16133263

    Open questions at the time
    • Discrepancy between random-order and ordered binding models across the two studies
    • Structural basis of the translocation cycle not determined
  3. 2009 Medium

    Identified tissue-specific ancillary proteins required for surface delivery, explaining why the transporter functions differently in kidney versus intestine.

    Evidence Heterologous co-expression of collectrin/TMEM27 and ACE2 in oocytes and cell lines (review synthesis)

    PMID:19472175

    Open questions at the time
    • Molecular interaction interface not mapped
    • Review-level synthesis rather than single primary dataset
  4. 2010 Medium

    Showed acute kinase regulation by SGK isoforms acts by stabilizing transporter at the membrane rather than altering catalysis.

    Evidence Voltage-clamp, surface protein quantification, and brefeldin A insertion-block in oocytes

    PMID:20511718

    Open questions at the time
    • Direct phosphorylation site on SLC6A19 not identified
    • Physiological context of SGK regulation untested in vivo
  5. 2011 Medium

    JAK2 was added as a regulator acting through increased transporter insertion, with a kinase-dead control establishing catalytic dependence.

    Evidence Voltage-clamp, chemiluminescence surface quantification, BFA block, K882E kinase-dead mutant in oocytes

    PMID:21964291

    Open questions at the time
    • Direct substrate phosphorylation not shown
    • Relevance to JAK2-V617F disease states unexplored
  6. 2011 High

    Established the systemic physiological consequence of losing the transporter, linking epithelial amino acid uptake to body weight, insulin secretion, and nutrient signaling.

    Evidence Slc6a19 knockout mouse with brush-border vesicle transport assays, insulin measurements, and mTOR/GCN2-ATF4 pathway analysis

    PMID:21636576

    Open questions at the time
    • Tissue-specific contributions to phenotype not dissected
    • Mechanism connecting transport loss to mTOR not resolved at molecular level
  7. 2012 High

    Revealed that the transporter operates within a brush-border digestive complex where peptidases shape its kinetic behavior.

    Evidence Reciprocal co-IP and blue-native electrophoresis of brush-border membranes, oocyte co-expression, APN catalytic-site mutagenesis

    PMID:22677001

    Open questions at the time
    • Stoichiometry of the multi-protein complex not defined here
    • In vivo physiological role of APN coupling untested
  8. 2012 Medium

    Extended kinase regulation to PKB/Akt acting cooperatively with PIKfyve to promote membrane insertion.

    Evidence Voltage-clamp with wild-type and inactive kinase mutants plus BFA block in oocytes

    PMID:23234856

    Open questions at the time
    • Direct phosphorylation target unidentified
    • Single lab, oocyte-only system
  9. 2013 Medium

    Defined how spatial expression along the crypt-villus axis is set, integrating DNA methylation, histone marks, and transcription factors.

    Evidence Crypt/villus fractionation, bisulfite sequencing, H3K27Ac ChIP, and HNF1a/HNF4a/SOX9 manipulation

    PMID:24121511

    Open questions at the time
    • Upstream signals controlling these epigenetic states unknown
    • Conservation of regulation in human tissue untested
  10. 2014 Medium

    Provided a pharmacological tool and inhibitor binding model, supporting an external blocking site on the translocation path.

    Evidence Proteoliposome Na+-glutamine co-transport inhibition kinetics and molecular docking with a homology model

    PMID:24704252

    Open questions at the time
    • Inhibitor binding site not experimentally validated
    • Docking based on homology model lacking experimental structure
  11. 2015 High

    Mapped specific collectrin-interacting residues and showed membrane delivery and catalytic activation are separable functions.

    Evidence Fusion constructs, mutagenesis screening, electrophysiology, and surface expression in oocytes; syntaxin competition

    PMID:26240152

    Open questions at the time
    • Structural detail of the collectrin contact face not solved
    • Syntaxin regulation in native epithelium untested
  12. 2021 Medium

    Determined the functional transport unit in native membranes, showing one ACE2:B0AT1 heterodimer suffices within the larger assembly.

    Evidence Radiation inactivation analysis of enterocyte brush-border membrane vesicles with target-theory mass calculation

    PMID:34847569

    Open questions at the time
    • Single method and single lab
    • Role of the higher-order dimer-of-heterodimers in function unclear
  13. 2022 Medium

    Extended the transporter's role beyond epithelia, showing it supplies proline to early embryos and supports fertility.

    Evidence Slc6a19 knockout mouse with radiolabeled L-proline uptake and amino acid competition assays in embryos

    PMID:36611813

    Open questions at the time
    • Mechanism linking proline uptake to embryo development not defined
    • Human relevance of embryonic expression untested
  14. 2025 Medium

    Clarified the molecular pathology of Hartnup variants as ER retention, and showed some variants impair ACE2 trafficking.

    Evidence Subcellular localization assays and in silico analysis of 18 disease variants

    PMID:40852587

    Open questions at the time
    • Whether ER retention is rescuable not addressed
    • Functional consequence of ACE2 mistrafficking not quantified
  15. 2025 Medium

    Implicated the transporter in cancer biology via tryptophan-fueled NAD+/SIRT1 signaling that suppresses EMT in renal carcinoma.

    Evidence SLC6A19 overexpression in RCC cells with NAD+ measurement, SIRT1 activity, H3K27ac ChIP, NF-kB and KLF4 analyses

    PMID:41203631

    Open questions at the time
    • Causal chain rests on overexpression rather than endogenous modulation
    • Generalizability beyond RCC unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • An experimentally determined high-resolution structure of the transport cycle and a unifying model reconciling ordered versus random substrate binding remain open.
  • No experimental structure of the human transporter in the corpus
  • Direct phosphorylation sites underlying kinase regulation unidentified
  • In vivo significance of kinase regulation untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0140104 molecular carrier activity 2
Localization
GO:0005886 plasma membrane 6 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-382551 Transport of small molecules 3 R-HSA-1643685 Disease 2 R-HSA-8963743 Digestion and absorption 2
Partners
ACE2AKT1APNJAK2SGK1STX1ASTX3TMEM27
Complex memberships
ACE2:B0AT1 heterodimer (dimer-of-heterodimers)B0AT1-APN-ACE2 brush-border digestive complexcollectrin (TMEM27):B0AT1 complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 SLC6A19 (B0AT1) encodes a sodium-dependent, chloride-independent neutral amino acid transporter expressed predominantly in kidney and intestine; disease-causing mutations reduce neutral amino acid transport function in vitro, establishing it as the gene mutated in Hartnup disorder. Positional cloning, mutation identification, in vitro transport assays in heterologous expression systems Nature genetics High 15286787 15286788
2005 Mouse B0AT1 mediates electrogenic Na+-amino acid co-transport with 1:1 stoichiometry; all neutral amino acids are substrates but large neutral non-aromatic amino acids are preferred; no other ions are involved in the transport mechanism; a random binding order model with a positive charge on the ternary [Na+-substrate-transporter] complex is consistent with experimental data. Two-electrode voltage-clamp and tracer studies in Xenopus oocyte expression system The Biochemical journal High 15804236
2005 Mouse B0AT1 transports one Na+ per neutral amino acid via an ordered, simultaneous mechanism in which the amino acid binds prior to Na+, followed by simultaneous translocation; Li+ can partially substitute for Na+; Cl- and H+ influence current magnitude. Two-electrode voltage-clamp with simultaneous charge translocation and radiolabeled amino acid uptake measurements in Xenopus oocytes Pflugers Archiv : European journal of physiology High 16133263
2009 SLC6A19 requires either collectrin (TMEM27) or angiotensin-converting enzyme 2 (ACE2) for surface expression in the kidney and intestine, respectively. Heterologous expression in Xenopus oocytes and cell lines with co-expression of ancillary proteins; review synthesizing experimental findings IUBMB life Medium 19472175
2010 SGK1, SGK2, and SGK3 stimulate SLC6A19 transport activity by increasing cell surface expression of the transporter (higher Vmax without changing substrate affinity); SGK stabilizes the transporter in the plasma membrane rather than increasing insertion rate; ACE2 co-expression markedly increases SLC6A19 currents and is further enhanced by SGK isoforms. Two-electrode voltage-clamp in Xenopus oocytes, quantitative immunoassay for surface protein, brefeldin A insertion-block experiments Cellular physiology and biochemistry Medium 20511718
2011 Mice lacking B0AT1 (Slc6a19-/-) show complete abolition of Na+-dependent neutral amino acid uptake in intestinal and renal brush-border membrane vesicles; these mice exhibit reduced body weight, blunted postprandial insulin secretion, reduced intestinal mTOR pathway signaling, and activation of the GCN2/ATF4 stress response pathway, demonstrating that epithelial neutral amino acid uptake is essential for body weight regulation and nutrient signaling. Slc6a19 knockout mouse model; brush-border membrane vesicle transport assays; insulin secretion measurements; mTOR and GCN2/ATF4 pathway analysis The Journal of biological chemistry High 21636576
2011 JAK2 (and gain-of-function V617F-JAK2) stimulates SLC6A19 transport activity by increasing carrier protein abundance at the cell membrane (higher Vmax, unchanged affinity); kinase-dead K882E-JAK2 has no effect; JAK2 stimulates transporter insertion into rather than inhibiting retrieval from the plasma membrane. Two-electrode voltage-clamp in Xenopus oocytes, chemiluminescence surface protein quantification, brefeldin A insertion-block experiments Biochemical and biophysical research communications Medium 21964291
2012 B0AT1 forms functional complexes with the peptidases aminopeptidase N (APN/CD13) and ACE2 in intestinal brush-border membranes; APN increases B0AT1 substrate affinity up to 2.5-fold and increases surface expression; site-directed mutagenesis of APN's catalytic site suggests it increases local substrate concentration to modulate apparent affinity. Co-immunoprecipitation and Blue native electrophoresis of intestinal brush-border membrane proteins; Xenopus oocyte co-expression electrophysiology; site-directed mutagenesis of APN The Biochemical journal High 22677001
2012 PKB/Akt stimulates SLC6A19 transport activity by increasing maximal transport rate (Vmax) without altering substrate affinity; this effect is augmented by PIKfyve in a PKB/Akt phosphorylation-dependent manner; PKB/Akt promotes transporter insertion into the plasma membrane rather than inhibiting retrieval. Two-electrode voltage-clamp in Xenopus oocytes with wild-type and inactive mutant kinases; brefeldin A insertion-block experiments Cellular physiology and biochemistry Medium 23234856
2013 Slc6a19 gene expression in intestinal enterocytes is regulated at three levels: CpG dinucleotides in the proximal promoter are highly methylated in crypt cells and fully demethylated in villus cells; histone H3K27Ac (active promoter mark) is present in villus but not crypt cells; transcription factors HNF1a and HNF4a activate transcription in villus enterocytes while SOX9 represses expression in crypts. Fractionation of crypt vs villus enterocytes; bisulfite sequencing for DNA methylation; ChIP for H3K27Ac; gene expression analysis with transcription factor manipulation The Journal of biological chemistry Medium 24121511
2014 Nimesulide is a potent inhibitor of B0AT1 (IC50 ~23 μM in proteoliposomes); it shows noncompetitive inhibition with respect to glutamine but competitive inhibition with respect to Na+; molecular docking suggests nimesulide binds an external site on B0AT1, sterically blocking the translocation path. Proteoliposome Na+-[3H]glutamine co-transport assay; inhibition kinetics analysis; molecular docking using B0AT1 homology model Biochemical pharmacology Medium 24704252
2015 Collectrin is necessary for both plasma membrane expression and catalytic function of B0AT1 and B0AT3; syntaxin 1A and syntaxin 3 inhibit B0AT1 membrane expression by competing with collectrin; mutagenesis screening identified residues on transmembrane domains 1α, 5, and 7 on one face of B0AT3 as key for collectrin interaction, with distinct residues mediating membrane expression vs. catalytic activation. Monocarboxylate-B0AT1/3 fusion constructs in Xenopus oocytes; mutagenesis screening; electrophysiology and surface expression assays The Journal of biological chemistry High 26240152
2021 Each [ACE2:B0AT1] heterodimer constitutes a functional unit for Na+-dependent neutral amino acid transport in situ; radiation inactivation analysis of brush-border membrane vesicles yielded a functional unit molecular weight of 183.7 ± 16.8 kDa, consistent with one ACE2:B0AT1 heterodimer acting as the transport unit within the larger ~345 kDa dimer-of-heterodimers quaternary complex. Radiation inactivation analysis using high-energy electron radiation from a linear accelerator on purified enterocyte brush-border membrane vesicles; target theory molecular weight calculation Function (Oxford, England) Medium 34847569
2022 B0AT1 is expressed in mouse preimplantation embryos along with ACE2; B0AT1 knockout mice show decreased fertility and reduced preimplantation embryo development; B0AT1 mediates the majority of L-proline uptake at the 4-8 cell stage; transport competition experiments confirm B0AT1 substrate specificity in embryos. Slc6a19 knockout mouse; radiolabeled L-proline uptake in oocytes and embryos; competition assays with unlabeled amino acids Cells Medium 36611813
2025 Nine Hartnup disease-causing B0AT1 variants (R57C, G93R, R95P, R178Q, L242P, G284R, S303L, D517G, P579L) are retained in the endoplasmic reticulum and fail to traffic to the plasma membrane; ER-retained variants R178Q and S303L also significantly disrupt ACE2 intracellular trafficking and its localization to the plasma membrane. Subcellular localization assays (biochemical fractionation and immunofluorescence) of 18 B0AT1 variants; in silico analysis Frontiers in cell and developmental biology Medium 40852587
2025 SLC6A19 transports tryptophan into renal cell carcinoma cells, facilitating de novo NAD+ biosynthesis which activates SIRT1; SIRT1 deacetylates histone H3K27, repressing NF-κB p65 transcription and suppressing epithelial-mesenchymal transition; KLF4 inactivation is identified as the key factor for low SLC6A19 expression in RCC cells. Overexpression of SLC6A19 in RCC cells; in vitro and in vivo proliferation/migration/invasion assays; NAD+ measurement; SIRT1 activity assay; H3K27 acetylation ChIP; NF-κB pathway analysis; KLF4 transcription factor binding assays Oncogenesis Medium 41203631

Source papers

Stage 0 corpus · 49 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Mutations in SLC6A19, encoding B0AT1, cause Hartnup disorder. Nature genetics 212 15286787
2004 Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. Nature genetics 185 15286788
2005 Characterization of mouse amino acid transporter B0AT1 (slc6a19). The Biochemical journal 106 15804236
2009 The role of the neutral amino acid transporter B0AT1 (SLC6A19) in Hartnup disorder and protein nutrition. IUBMB life 73 19472175
2011 Impaired nutrient signaling and body weight control in a Na+ neutral amino acid cotransporter (Slc6a19)-deficient mouse. The Journal of biological chemistry 69 21636576
2005 Steady-state kinetic characterization of the mouse B(0)AT1 sodium-dependent neutral amino acid transporter. Pflugers Archiv : European journal of physiology 55 16133263
2010 The serum and glucocorticoid inducible kinases SGK1-3 stimulate the neutral amino acid transporter SLC6A19. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 52 20511718
2012 Intestinal peptidases form functional complexes with the neutral amino acid transporter B(0)AT1. The Biochemical journal 51 22677001
2017 Identification of novel inhibitors of the amino acid transporter B0 AT1 (SLC6A19), a potential target to induce protein restriction and to treat type 2 diabetes. British journal of pharmacology 47 28176326
2017 Expression and regulation of the neutral amino acid transporter B0AT1 in rat small intestine. PloS one 47 28915252
2015 Molecular basis for the interaction of the mammalian amino acid transporters B0AT1 and B0AT3 with their ancillary protein collectrin. The Journal of biological chemistry 41 26240152
2010 Luminal leptin inhibits L-glutamine transport in rat small intestine: involvement of ASCT2 and B0AT1. American journal of physiology. Gastrointestinal and liver physiology 37 20448142
2012 Up-regulation of amino acid transporter SLC6A19 activity and surface protein abundance by PKB/Akt and PIKfyve. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 35 23234856
2022 Aristolochic acid-induced nephropathy is attenuated in mice lacking the neutral amino acid transporter B0AT1 (Slc6a19). American journal of physiology. Renal physiology 29 35979966
2014 Nimesulide binding site in the B0AT1 (SLC6A19) amino acid transporter. Mechanism of inhibition revealed by proteoliposome transport assay and molecular modelling. Biochemical pharmacology 28 24704252
2019 Mice Lacking the Intestinal and Renal Neutral Amino Acid Transporter SLC6A19 Demonstrate the Relationship between Dietary Protein Intake and Amino Acid Malabsorption. Nutrients 27 31470570
2010 Novel mutation in SLC6A19 causing late-onset seizures in Hartnup disorder. Pediatric neurology 25 20399395
2013 Enterocyte-specific regulation of the apical nutrient transporter SLC6A19 (B(0)AT1) by transcriptional and epigenetic networks. The Journal of biological chemistry 24 24121511
2011 Na-glutamine co-transporters B(0)AT1 in villus and SN2 in crypts are differentially altered in chronically inflamed rabbit intestine. Biochimica et biophysica acta 24 22100603
2018 Development of Biomarkers for Inhibition of SLC6A19 (B⁰AT1)-A Potential Target to Treat Metabolic Disorders. International journal of molecular sciences 23 30441827
2018 Identification and Characterization of Inhibitors of a Neutral Amino Acid Transporter, SLC6A19, Using Two Functional Cell-Based Assays. SLAS discovery : advancing life sciences R & D 22 30589598
2015 Intestinal B(0)AT1 (SLC6A19) and PEPT1 (SLC15A1) mRNA levels in European sea bass (Dicentrarchus labrax) reared in fresh water and fed fish and plant protein sources. Journal of nutritional science 22 26097704
2021 B0AT1 Amino Acid Transporter Complexed With SARS-CoV-2 Receptor ACE2 Forms a Heterodimer Functional Unit: In Situ Conformation Using Radiation Inactivation Analysis. Function (Oxford, England) 19 34847569
2022 Unconventional Functions of Amino Acid Transporters: Role in Macropinocytosis (SLC38A5/SLC38A3) and Diet-Induced Obesity/Metabolic Syndrome (SLC6A19/SLC6A14/SLC6A6). Biomolecules 18 35204736
2022 ACE2, B0AT1, and SARS-CoV-2 spike protein: Structural and functional implications. Current opinion in structural biology 18 35584583
2015 Mast cell regulation of Na-glutamine co-transporters B0AT1 in villus and SN2 in crypt cells during chronic intestinal inflammation. BMC gastroenterology 18 25884559
2008 Minisatellite polymorphisms of the SLC6A19: susceptibility in hypertension. Biochemical and biophysical research communications 18 18671945
2020 Repurposing Nimesulide, a Potent Inhibitor of the B0AT1 Subunit of the SARS-CoV-2 Receptor, as a Therapeutic Adjuvant of COVID-19. SLAS discovery : advancing life sciences R & D 17 32500793
2011 Stimulation of the amino acid transporter SLC6A19 by JAK2. Biochemical and biophysical research communications 17 21964291
2009 A novel missense mutation in the SLC6A19 gene in a Chinese family with Hartnup disorder. International journal of dermatology 14 19335424
2016 Amino acid transporter B(0)AT1 (slc6a19) and ancillary protein: impact on function. Pflugers Archiv : European journal of physiology 13 27255547
2018 Cyclooxygenase pathway mediates the inhibition of Na-glutamine co-transporter B0AT1 in rabbit villus cells during chronic intestinal inflammation. PloS one 10 30192835
2020 Low temperature bacterial expression of the neutral amino acid transporters SLC1A5 (ASCT2), and SLC6A19 (B0AT1). Molecular biology reports 9 32772343
2018 SLC6A19 is a novel putative gene, induced by dioxins via AhR in human hepatoma HepG2 cells. Environmental pollution (Barking, Essex : 1987) 9 29522993
2023 New aspects for the brain in Hartnup disease based on mining of high-resolution cellular mRNA expression data for SLC6A19. IBRO neuroscience reports 7 37101820
2022 Excretion of excess nitrogen and increased survival by loss of SLC6A19 in a mouse model of ornithine transcarbamylase deficiency. Journal of inherited metabolic disease 6 36220785
2007 Organ specific underexpression renal of Na+-dependent B0AT1 in the SHR correlates positively with overexpression of NHE3 and salt intake. Molecular and cellular biochemistry 6 17646927
2022 Stage-Specific L-Proline Uptake by Amino Acid Transporter Slc6a19/B0AT1 Is Required for Optimal Preimplantation Embryo Development in Mice. Cells 5 36611813
2021 Knockout of the Amino Acid Transporter SLC6A19 and Autoimmune Diabetes Incidence in Female Non-Obese Diabetic (NOD) Mice. Metabolites 5 34677380
2016 Expression of apical Na(+)-L-glutamine co-transport activity, B(0)-system neutral amino acid co-transporter (B(0)AT1) and angiotensin-converting enzyme 2 along the jejunal crypt-villus axis in young pigs fed a liquid formula. Amino acids 5 26984322
2018 Study of Seizure-Manifested Hartnup Disorder Case Induced By Novel Mutations in SLC6A19. Open life sciences 3 33817063
2025 Structural Dynamics of Neutral Amino Acid Transporter SLC6A19 in Simple and Complex Lipid Bilayers. Journal of cellular biochemistry 2 39749651
2025 Hartnup disease-causing SLC6A19 mutations lead to B0AT1 aberrant trafficking and ACE2 mis-localisation implicating the endoplasmic reticulum protein quality control. Frontiers in cell and developmental biology 2 40852587
2025 Interaction of B0AT1 Deficiency and Diet on Metabolic Function and Diabetes Incidence in Male Nonobese Diabetic Mice. Endocrinology 1 39844660
2025 MT1H inhibits the growth of gastric cancer by regulating SLC6A19/TTC39B/ADM2 and activating p53-dependent autophagy. Scientific reports 1 40102553
2022 The SLC6A19 gene mutation in a young man with hyperglycinuria and nephrolithiasis: a case report and literature review. BMC urology 1 36434624
2025 Engineering and immobilization of imine reductase enable chemoenzymatic synthesis of SLC6A19 inhibitor JNT-517. Bioresource technology 0 41027489
2025 SLC6A19-mediated tryptophan uptake suppresses renal cell carcinoma metastasis via activating NAD+-dependent deacetylase SIRT1. Oncogenesis 0 41203631
2023 Correction: Cyclooxygenase pathway mediates the inhibition of Na-glutamine co-transporter B0AT1 in rabbit villus cells during chronic intestinal inflammation. PloS one 0 37943850

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