Component

Human sodium-coupled neutral amino acid transporter 2 / SLC38A2

Context-specific entity; species, compartment and exposure are stated on each claim.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. SLC38A2 mediated alanine and glutamine uptake in human lung fibroblasts and increased with TGF-beta exposure or alanine deprivation.

    Human sodium-coupled neutral amino acid transporter 2 / SLC38A2 → Alanine availability in human lung fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Normal and IPF human lung fibroblast transporter experiments.
    limitations
    Dual transport does not by itself prove clinically relevant competition at ordinary plasma concentrations.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    A shared importer links access to two amino acids.
    primary_references
    TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 504–510

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Normal and IPF human lung fibroblast transporter experiments. · source_derived_draft · unverified_draft

    ## alanine-fibroblast-transporter A shared importer links access to two amino acids. SLC38A2 mediated alanine and glutamine uptake in human lung fibroblasts and increased with TGF-beta exposure or alanine deprivation. Model: Normal and IPF human lung fibroblast transporter experiments. Limitations: Dual transport does not by itself prove clinically relevant competition at ordinary plasma concentrations. Evidence access: Primary full text TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
    Complete structured claim and evidence

  2. Loss of SLC38A2 prevented human PDAC cells from effectively taking up and concentrating environmental alanine.

    Human sodium-coupled neutral amino acid transporter 2 / SLC38A2 → Intracellular alanine concentration in human PDAC cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC genetic transporter perturbation and stable-isotope flux assays.
    limitations
    Tissue-specific transporter dependence; not every cell uses SLC38A2 as its dominant route.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    An intact uptake system can be as important as having alanine outside the cell.
    primary_references
    Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 184–190

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC genetic transporter perturbation and stable-isotope flux assays. · source_derived_draft · unverified_draft

    ## alanine-pdac-snat2 An intact uptake system can be as important as having alanine outside the cell. Loss of SLC38A2 prevented human PDAC cells from effectively taking up and concentrating environmental alanine. Model: Human PDAC genetic transporter perturbation and stable-isotope flux assays. Limitations: Tissue-specific transporter dependence; not every cell uses SLC38A2 as its dominant route. Evidence access: Primary full text Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Combined inhibition of alanine synthesis and uptake suppressed fibrogenic responses in human fibroblasts and precision-cut lung slices.

    Combined alanine synthesis and uptake blockade → Human lung myofibroblast differentiation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cells and ex vivo lung tissue; metabolic perturbations.
    limitations
    Preclinical work, not an established human antifibrotic therapy. The final paper and its preprint are one study lineage.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Blocking both supply routes had a stronger mechanistic rationale than assuming only one route mattered.
    primary_references
    TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 528–534

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cells and ex vivo lung tissue; metabolic perturbations. · source_derived_draft · unverified_draft

    ## alanine-fibroblast-dual-block Blocking both supply routes had a stronger mechanistic rationale than assuming only one route mattered. Combined inhibition of alanine synthesis and uptake suppressed fibrogenic responses in human fibroblasts and precision-cut lung slices. Model: Human cells and ex vivo lung tissue; metabolic perturbations. Limitations: Preclinical work, not an established human antifibrotic therapy. The final paper and its preprint are one study lineage. Evidence access: Primary full text TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
    Complete structured claim and evidence

  2. SLC38A2-deficient PDAC cells increased de novo alanine synthesis and passive efflux, diverting mitochondrial pyruvate and amino-nitrogen sources toward alanine production.

    SLC38A2 loss in human PDAC cells → De novo alanine synthesis in human PDAC cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC flux and compartmental metabolism experiments.
    limitations
    Reported metabolic crisis is not a universal consequence of reduced dietary alanine.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Losing uptake can force a cell to spend other nutrients making the missing amino acid.
    primary_references
    Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 192–198

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC flux and compartmental metabolism experiments. · source_derived_draft · unverified_draft

    ## alanine-pdac-snat2-carbon-cost Losing uptake can force a cell to spend other nutrients making the missing amino acid. SLC38A2-deficient PDAC cells increased de novo alanine synthesis and passive efflux, diverting mitochondrial pyruvate and amino-nitrogen sources toward alanine production. Model: Human PDAC flux and compartmental metabolism experiments. Limitations: Reported metabolic crisis is not a universal consequence of reduced dietary alanine. Evidence access: Primary full text Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    Complete structured claim and evidence

  3. Genetic SLC38A2 suppression impaired human PDAC tumor growth and the support provided by co-injected stellate cells in mouse xenograft experiments.

    SLC38A2 loss in human PDAC cells → Human PDAC xenograft growth in mice source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC cells in immunodeficient mice; transporter perturbation.
    limitations
    Preclinical tumor dependency, not clinical efficacy or proof that alanine restriction is beneficial.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    A local nutrient-import dependency persisted in the animal tumor model.
    primary_references
    Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 208–214

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC cells in immunodeficient mice; transporter perturbation. · source_derived_draft · unverified_draft

    ## alanine-pdac-tumor-transporter A local nutrient-import dependency persisted in the animal tumor model. Genetic SLC38A2 suppression impaired human PDAC tumor growth and the support provided by co-injected stellate cells in mouse xenograft experiments. Model: Human PDAC cells in immunodeficient mice; transporter perturbation. Limitations: Preclinical tumor dependency, not clinical efficacy or proof that alanine restriction is beneficial. Evidence access: Primary full text Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32341021/ · DOI 10.1158/2159-8290.CD-19-0959
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards