Component

ERK1/2 proteins, isoform not resolved

ERK1/2 proteins, isoform not resolved. Species, exposure and limitations are retained in each linked claim.

4 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

Where it participates (unsigned role)

  1. Berberine increased LDLR expression through an ERK-dependent, SREBP-independent post-transcriptional mechanism in human hepatoma cells.

    Berberine → Human low-density lipoprotein receptor / LDLR source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/15531889.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac2a9817f85e5c1f4f520590f1f2cb1ca820cce75b79120852f616f7ce5bea2f", "start_char": 0, "end_char": 1032, "text_sha256": "ac2a9817f85e5c1f4f520590f1f2cb1ca820cce75b79120852f616f7ce5bea2f"}
    experimental_model
    Human hepatoma mRNA stability/promoter experiments, animal and small clinical arms
    exposure
    Berberine exposure with ERK-dependence assays
    limitations
    Clinical lipid outcomes do not directly prove this molecular route caused the human effect. Cell response was reported independent of SREBP.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human hepatoma cells for molecular claims
    plain_language
    More LDL receptor can help cells remove LDL from circulation; the mechanism was tested in cells.
    primary_references
    [berberine-p15531889] Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. (2004). https://pubmed.ncbi.nlm.nih.gov/15531889/ DOI: 10.1038/nm1135
    tissue_or_cell_type
    LDLR post-transcriptional regulation

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 454–465

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human hepatoma mRNA stability/promoter experiments, animal and small clinical arms · source_derived_draft · unverified_draft

    ### berberine-ldlr-protein Berberine increased LDLR expression through an ERK-dependent, SREBP-independent post-transcriptional mechanism in human hepatoma cells. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: More LDL receptor can help cells remove LDL from circulation; the mechanism was tested in cells. organism: Human hepatoma cells for molecular claims tissue_or_cell_type: LDLR post-transcriptional regulation experimental_model: Human hepatoma mRNA stability/promoter experiments, animal and small clinical arms limitations: Clinical lipid outcomes do not directly prove this molecular route caused the human effect. Cell response was reported independent of SREBP. exposure: Berberine exposure with ERK-dependence assays evidence_span: {"source_cache": "artifacts/berberine-research/15531889.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac2a9817f85e5c1f4f520590f1f2cb1ca820cce75b79120852f616f7ce5bea2f", "start_char": 0, "end_char": 1032, "text_sha256": "ac2a9817f85e5c1f4f520590f1f2cb1ca820cce75b79120852f616f7ce5bea2f"} [berberine-p15531889] Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. (2004). https://pubmed.ncbi.nlm.nih.gov/15531889/ DOI: 10.1038/nm1135
    Complete structured claim and evidence

  2. Erinacine C induced PC12 differentiation through TrkA and associated PLC-gamma, PI3K and ERK pathways.

    Erinacine C → TrkA-dependent PC12 differentiation source_derived_draftungraded
    Experimental context and source evidence
    dose
    Erinacine C with genetic and pharmacological inhibitors
    duration
    Differentiation assay
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    PC12 cells and astrocytic reporter cells
    limitations
    The study supports pathway involvement but not direct binding, human exposure, or a clinical neuroregenerative effect.
    nutrient_topic
    Hericenones & Erinacines chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Hericenones and erinacines
    organism
    PC12 cells and astrocytic reporter cells
    plain_language
    Erinacine C induced PC12 differentiation through TrkA and associated PLC-gamma, PI3K and ERK pathways.
    primary_references
    Erinacine C Activates Transcription from a Consensus ETS DNA Binding Site in Astrocytic Cells in Addition to NGF Induction. (2020). https://pubmed.ncbi.nlm.nih.gov/33066380/ DOI: 10.3390/biom10101440
    route
    In vitro
    tissue
    Neurotrophin-dependent differentiation

    Hericenones & Erinacines: mechanism of action and interactions (2026-09-20) · lines 88–97

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · PC12 cells and astrocytic reporter cells · source_derived_draft · unverified_draft

    ## hericenones-erinacines-erinacine-c-trka Erinacine C induced PC12 differentiation through TrkA and associated PLC-gamma, PI3K and ERK pathways. Model/species: PC12 cells and astrocytic reporter cells Tissue/system: Neurotrophin-dependent differentiation Exposure: Erinacine C with genetic and pharmacological inhibitors Route: In vitro Duration: Differentiation assay Limits: The study supports pathway involvement but not direct binding, human exposure, or a clinical neuroregenerative effect. Primary reference: Erinacine C Activates Transcription from a Consensus ETS DNA Binding Site in Astrocytic Cells in Addition to NGF Induction. (2020). https://pubmed.ncbi.nlm.nih.gov/33066380/ DOI: 10.3390/biom10101440 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation.

    K252a Trk-family inhibitor → Hericenone E potentiation of NGF-induced PC12 neuritogenesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Hericenone E with low NGF and K252a
    duration
    Differentiation assay
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Rat PC12 pheochromocytoma cells
    limitations
    Partial blockade suggests Trk involvement but not sole dependence; PC12 exposure does not establish human brain target engagement.
    nutrient_topic
    Hericenones & Erinacines chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Hericenones and erinacines
    organism
    Rat PC12 pheochromocytoma cells
    plain_language
    K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation.
    primary_references
    Hericium erinaceus (Bull.: Fr) Pers. cultivated under tropical conditions: isolation of hericenones and demonstration of NGF-mediated neurite outgrowth in PC12 cells via MEK/ERK and PI3K-Akt signaling pathways. (2014). https://pubmed.ncbi.nlm.nih.gov/25288148/ DOI: 10.1039/c4fo00452c
    route
    In vitro
    tissue
    NGF secretion, neurite outgrowth, ERK and Akt
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Hericenones & Erinacines: mechanism of action and interactions (2026-09-20) · lines 44–53

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Rat PC12 pheochromocytoma cells · source_derived_draft · unverified_draft

    ## hericenones-erinacines-hericenone-e-ngf K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation. Model/species: Rat PC12 pheochromocytoma cells Tissue/system: NGF secretion, neurite outgrowth, ERK and Akt Exposure: Hericenone E with low NGF and K252a Route: In vitro Duration: Differentiation assay Limits: Partial blockade suggests Trk involvement but not sole dependence; PC12 exposure does not establish human brain target engagement. Primary reference: Hericium erinaceus (Bull.: Fr) Pers. cultivated under tropical conditions: isolation of hericenones and demonstration of NGF-mediated neurite outgrowth in PC12 cells via MEK/ERK and PI3K-Akt signaling pathways. (2014). https://pubmed.ncbi.nlm.nih.gov/25288148/ DOI: 10.1039/c4fo00452c Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect.

    LY294002 → ARPE-19 survival after tert-butyl hydroperoxide challenge source_derived_draftungraded
    Experimental context and source evidence
    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
    Activating a pathway and needing it for protection are different tests.
    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

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 470–481

    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-pi3k-block LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activating a pathway and needing it for protection are different tests. 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

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