Component

67-kDa laminin receptor state / 67LR

Study-scoped entity; inspect species, exposure, model and limitations on each claim.

7 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. EGCG activation of 67LR increased cGMP, a rate-limiting signal for cell death in the model.

    67-kDa laminin receptor state / 67LR → Cyclic guanosine monophosphate source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Cancer-cell experiments and mouse xenografts in the 2013 study.
    limitations
    Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The receptor signal passed through cGMP.
    primary_references
    67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 60–66

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

    ## egcg-cgmp The receptor signal passed through cGMP. EGCG activation of 67LR increased cGMP, a rate-limiting signal for cell death in the model. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768
    Complete structured claim and evidence

  2. A genetic screen identified eEF1A as a component of 67LR-dependent EGCG signaling.

    67-kDa laminin receptor state / 67LR → Eukaryotic elongation factor 1A family source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Genetic screen, cell signaling and experimental tumor-growth models.
    limitations
    Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The surface signal depends on an intracellular relay.
    primary_references
    Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 28–34

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

    ## egcg-eef1a The surface signal depends on an intracellular relay. A genetic screen identified eEF1A as a component of 67LR-dependent EGCG signaling. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
    Complete structured claim and evidence

What acts on it

  1. Surface plasmon resonance supported nanomolar-affinity EGCG binding to 67LR; receptor expression conferred cellular responsiveness.

    Epigallocatechin-3-gallate (EGCG) → 67-kDa laminin receptor state / 67LR source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Receptor binding and cancer-cell expression experiments.
    limitations
    67LR is recorded as the receptor state, not equated with all functions of the 37-kDa RPSA precursor.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    A cell-surface receptor can make cells responsive to EGCG.
    primary_references
    A receptor for green tea polyphenol EGCG. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024383/ · DOI 10.1038/nsmb743

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 20–26

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Receptor binding and cancer-cell expression experiments. · source_derived_draft · unverified_draft

    ## egcg-receptor A cell-surface receptor can make cells responsive to EGCG. Surface plasmon resonance supported nanomolar-affinity EGCG binding to 67LR; receptor expression conferred cellular responsiveness. Model: Receptor binding and cancer-cell expression experiments. Limitations: 67LR is recorded as the receptor state, not equated with all functions of the 37-kDa RPSA precursor. Evidence access: primary abstract. A receptor for green tea polyphenol EGCG. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024383/ · DOI 10.1038/nsmb743
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Silencing MYPT1, eEF1A or 67LR abrogated EGCG-mediated tumor-growth inhibition in the tested models.

    Myosin phosphatase targeting subunit 1 family / MYPT1 → Tumor growth in EGCG experimental models source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Genetic screen, cell signaling and experimental tumor-growth models.
    limitations
    Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Removing pathway components prevented the observed response.
    primary_references
    Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 52–58

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

    ## egcg-machinery Removing pathway components prevented the observed response. Silencing MYPT1, eEF1A or 67LR abrogated EGCG-mediated tumor-growth inhibition in the tested models. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
    Complete structured claim and evidence

  2. EGCG dephosphorylated MYPT1 Thr696 through 67LR and eEF1A.

    Epigallocatechin-3-gallate (EGCG) → MYPT1 Thr696 phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Genetic screen, cell signaling and experimental tumor-growth models.
    limitations
    Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    EGCG removed an inhibitory phosphorylation mark in this pathway.
    primary_references
    Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 36–42

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

    ## egcg-mypt EGCG removed an inhibitory phosphorylation mark in this pathway. EGCG dephosphorylated MYPT1 Thr696 through 67LR and eEF1A. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
    Complete structured claim and evidence

  3. EGCG reduced TLR4 expression through 67LR.

    Epigallocatechin-3-gallate (EGCG) → TLR4 expression source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract.
    limitations
    Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The cells expressed less of the tested inflammatory receptor.
    primary_references
    TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 108–114

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. · source_derived_draft · unverified_draft

    ## egcg-tlr4 The cells expressed less of the tested inflammatory receptor. EGCG reduced TLR4 expression through 67LR. Model: Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. Limitations: Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation. Evidence access: primary abstract. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742
    Complete structured claim and evidence

  4. EGCG rapidly increased Tollip expression; 67LR silencing or antibody blockade prevented this.

    Epigallocatechin-3-gallate (EGCG) → Tollip expression source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract.
    limitations
    Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    EGCG increased a brake on inflammatory signaling.
    primary_references
    TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 100–106

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. · source_derived_draft · unverified_draft

    ## egcg-tollip EGCG increased a brake on inflammatory signaling. EGCG rapidly increased Tollip expression; 67LR silencing or antibody blockade prevented this. Model: Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. Limitations: Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation. Evidence access: primary abstract. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742
    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