Component

Experimental human STK11 / LKB1 siRNA knockdown

Experimental human STK11 / LKB1 siRNA knockdown. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation.

    Experimental human STK11 / LKB1 siRNA knockdown → Human acetyl-CoA carboxylase activity, isoform unresolved in assay source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    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
    Removing an upstream component interrupted the response.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 510–521

    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-acc LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. 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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [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

  2. LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation.

    Experimental human STK11 / LKB1 siRNA knockdown → Human AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    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
    Removing an upstream component interrupted the response.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 497–508

    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-ampk LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. 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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [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

  3. LKB1 knockdown blocked the triglyceride-lowering response to norathyriol.

    Experimental human STK11 / LKB1 siRNA knockdown → Triglyceride accumulation in human HepG2 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    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
    Removing an upstream component interrupted the response.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 484–495

    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-tg LKB1 knockdown blocked the triglyceride-lowering response to norathyriol. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. 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": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards