Component

Lysosome-associated AMPK activity

Lysosome-associated AMPK activity. 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.

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 acts on it

  1. AXIN1 loss impaired the berberine response of lysosomal AMPK.

    Human AXIN1 → Lysosome-associated AMPK activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/berberine-research/37144221.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d", "start_char": 0, "end_char": 1212, "text_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d"}
    experimental_model
    Lysosome isolation, genetic perturbation and coimmunoprecipitation
    exposure
    Low-dose berberine experiments; AXIN1 loss, PEN2 perturbation and UHRF1 overexpression
    limitations
    Cancer-cell signaling model; low laboratory concentration is not proof of a mechanism at every human tissue exposure. Different dose/context from respiratory inhibition studies.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human HCT-116 cells
    plain_language
    This branch cannot operate normally without its scaffold.
    primary_references
    [berberine-p37144221] Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. (2023). https://pubmed.ncbi.nlm.nih.gov/37144221/ DOI: 10.3389/fphar.2023.1148611
    tissue_or_cell_type
    Lysosomal AMPK and UHRF1 regulation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 415–426

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lysosome isolation, genetic perturbation and coimmunoprecipitation · source_derived_draft · unverified_draft

    ### berberine-axin1-loss AXIN1 loss impaired the berberine response of lysosomal AMPK. Condition category: machinery_impairment nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This branch cannot operate normally without its scaffold. organism: Human HCT-116 cells tissue_or_cell_type: Lysosomal AMPK and UHRF1 regulation experimental_model: Lysosome isolation, genetic perturbation and coimmunoprecipitation limitations: Cancer-cell signaling model; low laboratory concentration is not proof of a mechanism at every human tissue exposure. Different dose/context from respiratory inhibition studies. exposure: Low-dose berberine experiments; AXIN1 loss, PEN2 perturbation and UHRF1 overexpression evidence_span: {"source_cache": "artifacts/berberine-research/37144221.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d", "start_char": 0, "end_char": 1212, "text_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d"} [berberine-p37144221] Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. (2023). https://pubmed.ncbi.nlm.nih.gov/37144221/ DOI: 10.3389/fphar.2023.1148611
    Complete structured claim and evidence
  2. Berberine activated lysosome-associated AMPK in an AXIN1-dependent, PEN2-independent manner in HCT-116 cells.

    Berberine → Lysosome-associated AMPK activity source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/37144221.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d", "start_char": 0, "end_char": 1212, "text_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d"}
    experimental_model
    Lysosome isolation, genetic perturbation and coimmunoprecipitation
    exposure
    Low-dose berberine experiments; AXIN1 loss, PEN2 perturbation and UHRF1 overexpression
    limitations
    Cancer-cell signaling model; low laboratory concentration is not proof of a mechanism at every human tissue exposure. Different dose/context from respiratory inhibition studies.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human HCT-116 cells
    plain_language
    A lysosomal signaling route adds detail beyond a single mitochondrial explanation.
    primary_references
    [berberine-p37144221] Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. (2023). https://pubmed.ncbi.nlm.nih.gov/37144221/ DOI: 10.3389/fphar.2023.1148611
    tissue_or_cell_type
    Lysosomal AMPK and UHRF1 regulation

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 376–387

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lysosome isolation, genetic perturbation and coimmunoprecipitation · source_derived_draft · unverified_draft

    ### berberine-lysosomal-ampk Berberine activated lysosome-associated AMPK in an AXIN1-dependent, PEN2-independent manner in HCT-116 cells. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lysosomal signaling route adds detail beyond a single mitochondrial explanation. organism: Human HCT-116 cells tissue_or_cell_type: Lysosomal AMPK and UHRF1 regulation experimental_model: Lysosome isolation, genetic perturbation and coimmunoprecipitation limitations: Cancer-cell signaling model; low laboratory concentration is not proof of a mechanism at every human tissue exposure. Different dose/context from respiratory inhibition studies. exposure: Low-dose berberine experiments; AXIN1 loss, PEN2 perturbation and UHRF1 overexpression evidence_span: {"source_cache": "artifacts/berberine-research/37144221.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d", "start_char": 0, "end_char": 1212, "text_sha256": "e146553474cca4ec8441b54580959225dcf3dfee60a50ea519ccac5e2cb6488d"} [berberine-p37144221] Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. (2023). https://pubmed.ncbi.nlm.nih.gov/37144221/ DOI: 10.3389/fphar.2023.1148611
    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