Component
Human tyrosine-protein kinase FGR
Human tyrosine-protein kinase FGR
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 acts on it
Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay.
Experimental context and source evidence
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_model
- Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods.
- interpretation_status
- Recorded from source with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
- plain_language
- Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay.
- primary_references
- Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
- source_locator
- Reviewed reference api-fgr-binding; DARTS/CETSA in mouse and human macrophage preparations supplied additional association evidence. Docking alone was not treated as binding proof; no unverified numeric KD assigned.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 392–398
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods. · Recorded from source · Recorded from source
### api-fgr-binding Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay. DARTS/CETSA in mouse and human macrophage preparations supplied additional association evidence. Docking alone was not treated as binding proof; no unverified numeric KD assigned. Model and exposure: Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Where it participates (unsigned role)
Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.
Experimental context and source evidence
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_contrast
- {"intervention": "Apigenin before bacterial challenge", "comparator": "DMSO control", "endpoint": "Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- THP1-derived macrophages; apigenin treatment followed by E. coli stimulation.
- interpretation_status
- Recorded from source with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
- plain_language
- Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.
- primary_references
- Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
- source_locator
- Reviewed reference api-human-phagocytosis; Human cell-line evidence is not a human infection-outcome trial.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 448–454
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · THP1-derived macrophages; apigenin treatment followed by E. coli stimulation. · Recorded from source · Recorded from source
### api-human-phagocytosis Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages. Human cell-line evidence is not a human infection-outcome trial. Model and exposure: THP1-derived macrophages; apigenin treatment followed by E. coli stimulation. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
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.