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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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
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)
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 evidenceExpression 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 evidenceFisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.