Component

Mouse mechanistic target of rapamycin / Mtor

Mouse mechanistic target of rapamycin / Mtor. Species, exposure and limitations are retained in each linked claim.

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

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. Rapamycin reduced mouse intestinal antimicrobial peptides, and nicotinamide did not rescue that reduction.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, mTOR results and Supplementary Figure 22 description
    experimental_model
    Mouse mTOR inhibition in vivo.
    limitations
    Rapamycin affects multiple cell types; no human dietary threshold established.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    More precursor or downstream vitamin cannot replace every missing signal.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 98–104

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse mTOR inhibition in vivo. · source_derived_draft · unverified_draft

    ## tryptophan-mtor-block-nam More precursor or downstream vitamin cannot replace every missing signal. Rapamycin reduced mouse intestinal antimicrobial peptides, and nicotinamide did not rescue that reduction. Model: Mouse mTOR inhibition in vivo. Limitations: Rapamycin affects multiple cell types; no human dietary threshold established. Evidence access: Primary full text, mTOR results and Supplementary Figure 22 description ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

What acts on it

  1. Theanine exposure was associated with mTOR pathway activation and phosphorylation of downstream S6 and S6K1 in mice.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"}
    experimental_model
    Intestinal transporter and phosphorylation assays
    exposure
    Oral L-theanine supplementation in the mouse experiment
    limitations
    Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred.
    nutrient_topic
    L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
    organism
    Mice
    plain_language
    The signaling pathway and transporter changes occurred together; that alone does not prove the pathway caused every change.
    primary_references
    [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    tissue_or_cell_type
    Intestinal amino acid transport and mTOR signaling

    L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 718–729

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal transporter and phosphorylation assays · source_derived_draft · unverified_draft

    ### theanine-mouse-mtor Theanine exposure was associated with mTOR pathway activation and phosphorylation of downstream S6 and S6K1 in mice. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling pathway and transporter changes occurred together; that alone does not prove the pathway caused every change. organism: Mice tissue_or_cell_type: Intestinal amino acid transport and mTOR signaling experimental_model: Intestinal transporter and phosphorylation assays limitations: Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred. exposure: Oral L-theanine supplementation in the mouse experiment evidence_span: {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"} [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments.

    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 5
    experimental_model
    Mouse leukemia multiomics, signaling and metabolic experiments.
    limitations
    This pathway is not established as a universal response to taurine in healthy human cells.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Transport was connected to growth signaling and fuel use.
    primary_references
    Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 537–543

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia multiomics, signaling and metabolic experiments. · source_derived_draft · unverified_draft

    ## taurine-leukemia-mtor Transport was connected to growth signaling and fuel use. Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments. Model: Mouse leukemia multiomics, signaling and metabolic experiments. Limitations: This pathway is not established as a universal response to taurine in healthy human cells. Evidence access: Primary full text, Figure 5 Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
    Complete structured claim and evidence
  2. Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells.

    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 5p–s and associated results
    experimental_model
    Mouse leukemia expression-rescue experiments.
    limitations
    Rescue does not identify taurine as a direct physical ligand of RAGA.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    A downstream rescue tested the signaling chain.
    primary_references
    Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 545–551

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia expression-rescue experiments. · source_derived_draft · unverified_draft

    ## taurine-leukemia-rag-rescue A downstream rescue tested the signaling chain. Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells. Model: Mouse leukemia expression-rescue experiments. Limitations: Rescue does not identify taurine as a direct physical ligand of RAGA. Evidence access: Primary full text, Figure 5p–s and associated results Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
    Complete structured claim and evidence
  3. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling.

    Fisetin → Mouse C/EBP alpha / Cebpa source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Chromatin immunoprecipitation; comparison with rapamycin.
    limitations
    Association and phenocopy do not resolve every direct target.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    A transcriptional step links signaling to glucose transport.
    primary_references
    Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 304–310

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chromatin immunoprecipitation; comparison with rapamycin. · source_derived_draft · unverified_draft

    ## fisetin-adipocyte-promoter A transcriptional step links signaling to glucose transport. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling. Model: Chromatin immunoprecipitation; comparison with rapamycin. Limitations: Association and phenocopy do not resolve every direct target. Evidence access: Primary abstract Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821
    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