Component
AKT catalytic output in human U2OS cells
AKT catalytic output in human U2OS cells. Species, exposure and limitations are retained in each linked claim.
1 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
Reduced phosphorylation of the AKT substrate beta-catenin at S552 indicated lower AKT output despite increased AKT T308/S473 phosphorylation.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"}
- experimental_model
- Human cell experiments with CRISPR NRF2 deletion
- exposure
- Concentration- and time-dependent sulforaphane treatment
- limitations
- Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial.
- nutrient_topic
- Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
- organism
- Human U2OS osteosarcoma cells and NRF2-knockout counterpart
- plain_language
- An activation marker and the enzyme output moved in different directions.
- primary_references
- [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062
- tissue_or_cell_type
- HDAC6, AKT and mTOR signaling
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 658–669
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell experiments with CRISPR NRF2 deletion · source_derived_draft · unverified_draft
### sulforaphane-akt-output Reduced phosphorylation of the AKT substrate beta-catenin at S552 indicated lower AKT output despite increased AKT T308/S473 phosphorylation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An activation marker and the enzyme output moved in different directions. organism: Human U2OS osteosarcoma cells and NRF2-knockout counterpart tissue_or_cell_type: HDAC6, AKT and mTOR signaling experimental_model: Human cell experiments with CRISPR NRF2 deletion limitations: Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial. exposure: Concentration- and time-dependent sulforaphane treatment evidence_span: {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"} [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062
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.