Component
Human ATG5
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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
ATG5 knockdown in human pancreatic stellate cells reduced alanine concentrations in their conditioned medium.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human PSC shRNA experiments; serum-free conditioned medium.
- limitations
- Knockdown is machinery impairment, not low dietary alanine; residual secretion and other autophagy effects remain. Correction record: Publisher erratum corrects the second image label in Fig. 3a to hPSC-LC3 + 8988T, matching Fig. 3b; production labeling correction, not a retraction or independent study. https://www.nature.com/articles/nature19851.pdf
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- Disrupting one part of autophagy reduced alanine supplied by neighboring cells.
- primary_references
- Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27509858/ · DOI 10.1038/nature19084
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 144–150
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PSC shRNA experiments; serum-free conditioned medium. · source_derived_draft · unverified_draft
## alanine-psc-atg5 Disrupting one part of autophagy reduced alanine supplied by neighboring cells. ATG5 knockdown in human pancreatic stellate cells reduced alanine concentrations in their conditioned medium. Model: Human PSC shRNA experiments; serum-free conditioned medium. Limitations: Knockdown is machinery impairment, not low dietary alanine; residual secretion and other autophagy effects remain. Correction record: Publisher erratum corrects the second image label in Fig. 3a to hPSC-LC3 + 8988T, matching Fig. 3b; production labeling correction, not a retraction or independent study. https://www.nature.com/articles/nature19851.pdf Evidence access: Primary full text Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27509858/ · DOI 10.1038/nature19084
Complete structured claim and evidence
Where it participates (unsigned role)
AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- dose
- Naringenin with AMPK inhibition, Atg5 silencing or chloroquine
- duration
- Acute cell assay
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm
- limitations
- The inhibitor and silencing experiments support pathway dependence in this model, not rheumatoid-arthritis efficacy in humans.
- nutrient_topic
- Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
- organism
- LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm
- plain_language
- AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect.
- primary_references
- Naringenin ameliorates collagen-induced arthritis through activating AMPK-mediated autophagy in macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37904715/ DOI: 10.1002/iid3.983
- route
- In vitro perturbation
- tissue
- AMPK/ULK1 autophagic flux and cytokines
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Naringenin: mechanism of action and interactions (2026-09-20) · lines 132–141
Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm · source_derived_draft · unverified_draft
## naringenin-ampk-autophagy-dependence AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect. Model/species: LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm Tissue/system: AMPK/ULK1 autophagic flux and cytokines Exposure: Naringenin with AMPK inhibition, Atg5 silencing or chloroquine Route: In vitro perturbation Duration: Acute cell assay Limits: The inhibitor and silencing experiments support pathway dependence in this model, not rheumatoid-arthritis efficacy in humans. Primary reference: Naringenin ameliorates collagen-induced arthritis through activating AMPK-mediated autophagy in macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37904715/ DOI: 10.1002/iid3.983 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
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.