Component
LY294002
LY294002. Species, exposure and limitations are retained in each linked 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
LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
- experimental_model
- Cell challenge with siRNA and pathway inhibitors
- exposure
- Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
- limitations
- Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
- nutrient_topic
- Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
- organism
- Human ARPE-19 cell line
- plain_language
- Activating a pathway and needing it for protection are different tests.
- primary_references
- [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
- tissue_or_cell_type
- Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 470–481
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-pi3k-block LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activating a pathway and needing it for protection are different tests. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidenceLY294002 reversed nasunin-associated protection and worsened t-BHP cytotoxicity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
- experimental_model
- Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
- exposure
- Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
- limitations
- Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
- nutrient_topic
- Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
- organism
- Mouse MC3T3-E1 cells
- plain_language
- The pathway must remain functional for this observed protection.
- primary_references
- [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
- tissue_or_cell_type
- Survival, differentiation markers, redox state and Akt signaling
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 406–417
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft
### nasunin-bone-pi3k-dependence LY294002 reversed nasunin-associated protection and worsened t-BHP cytotoxicity. Condition category: machinery_impairment nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pathway must remain functional for this observed protection. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
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.