Component
Human LKB1 acetylation in HepG2 cells
Human LKB1 acetylation in HepG2 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
Norathyriol lowered measured LKB1 acetylation in HepG2 cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"}
- experimental_model
- KK-Ay mouse liver experiments and mechanistic HepG2 studies
- exposure
- Norathyriol in sodium-oleate lipid-loading model; micromolar range
- limitations
- Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
- nutrient_topic
- Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
- organism
- Homo sapiens for HepG2 experiments; mouse findings separately scoped
- plain_language
- A chemical modification of an upstream kinase changed.
- primary_references
- [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
- tissue_or_cell_type
- HepG2 cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 458–469
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-lkb1-acetylation Norathyriol lowered measured LKB1 acetylation in HepG2 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemical modification of an upstream kinase changed. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
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.