Component
Experimental human NFE2L2 knockdown
Experimental human NFE2L2 knockdown. 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
Nrf2 knockdown lowered survival under combined treatment from 82.4% to 51.1%.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/sulforaphane-research/26094214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de55004b06332873c312c03a18cec65eeb22c1bab6daddf5cde8a7977817567e", "start_char": 0, "end_char": 1568, "text_sha256": "de55004b06332873c312c03a18cec65eeb22c1bab6daddf5cde8a7977817567e"}
- experimental_model
- Combination treatment and siRNA loss-of-function
- exposure
- Sulforaphane plus selenium with Nrf2 or TXNRD1 knockdown
- limitations
- One cell model; survival percentages are assay-specific and not clinical benefit estimates.
- nutrient_topic
- Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
- organism
- Human nontransformed CCD841 colonic cells
- plain_language
- The regulator was necessary for much of the observed protection.
- primary_references
- [sulforaphane-p26094214] Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells. (2015). https://pubmed.ncbi.nlm.nih.gov/26094214/ DOI: 10.1016/j.nutres.2015.05.011
- tissue_or_cell_type
- Nrf2/TXNRD1 and peroxide survival
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 788–799
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Combination treatment and siRNA loss-of-function · source_derived_draft · unverified_draft
### sulforaphane-nrf2-knockdown Nrf2 knockdown lowered survival under combined treatment from 82.4% to 51.1%. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The regulator was necessary for much of the observed protection. organism: Human nontransformed CCD841 colonic cells tissue_or_cell_type: Nrf2/TXNRD1 and peroxide survival experimental_model: Combination treatment and siRNA loss-of-function limitations: One cell model; survival percentages are assay-specific and not clinical benefit estimates. exposure: Sulforaphane plus selenium with Nrf2 or TXNRD1 knockdown evidence_span: {"source_cache": "artifacts/sulforaphane-research/26094214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de55004b06332873c312c03a18cec65eeb22c1bab6daddf5cde8a7977817567e", "start_char": 0, "end_char": 1568, "text_sha256": "de55004b06332873c312c03a18cec65eeb22c1bab6daddf5cde8a7977817567e"} [sulforaphane-p26094214] Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells. (2015). https://pubmed.ncbi.nlm.nih.gov/26094214/ DOI: 10.1016/j.nutres.2015.05.011
Complete structured claim and evidenceNrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- 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
- Adding pigment could not fully replace the missing regulatory machinery.
- 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
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 444–455
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-nrf2-failure Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding pigment could not fully replace the missing regulatory machinery. 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 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.