Component

Human insulin receptor substrate 1 / IRS1

Human insulin receptor substrate 1 / IRS1. Species, exposure and limitations are retained in each linked claim.

5 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. After vanadyl treatment, muscle showed trends toward increased basal insulin-receptor, IRS1 and Shc tyrosine phosphorylation and IRS1-associated PI3K activity without additional insulin-stimulated increases.

    Vanadyl sulfate → Insulin receptor / INSR source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human muscle samples from the same 16-person trial.
    limitations
    Reported as trends; phosphorylation patterns did not clearly correlate with glucose disposal. No proven nutrient requirement.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Early signaling markers did not guarantee a larger response to insulin.
    primary_references
    Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10726921/ · DOI 10.1016/s0026-0495(00)90418-9

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 390–396

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human muscle samples from the same 16-person trial. · source_derived_draft · unverified_draft

    ## vanadium-human-signaling Early signaling markers did not guarantee a larger response to insulin. After vanadyl treatment, muscle showed trends toward increased basal insulin-receptor, IRS1 and Shc tyrosine phosphorylation and IRS1-associated PI3K activity without additional insulin-stimulated increases. Model: Human muscle samples from the same 16-person trial. Limitations: Reported as trends; phosphorylation patterns did not clearly correlate with glucose disposal. No proven nutrient requirement. Evidence access: Primary abstract Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10726921/ · DOI 10.1016/s0026-0495(00)90418-9
    Complete structured claim and evidence

  2. Lycopene reduced IGF-I-stimulated AP-1 binding capacity in MCF7 cells.

    Lycopene → AP-1 DNA-binding capacity in human MCF7 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}
    experimental_model
    Growth-factor stimulation and signaling assays
    exposure
    IGF-I stimulation with lycopene exposure
    limitations
    Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human MCF7 breast cancer cells
    plain_language
    A downstream gene-regulatory response also fell.
    primary_references
    [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    tissue_or_cell_type
    IRS1 phosphorylation, AP-1 and cell cycle

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 676–687

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

    ### lycopene-ap1 Lycopene reduced IGF-I-stimulated AP-1 binding capacity in MCF7 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A downstream gene-regulatory response also fell. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    Complete structured claim and evidence

  3. Lycopene delayed cell-cycle progression without accompanying apoptotic or necrotic cell death in the tested MCF7 cultures.

    Lycopene → MCF7 breast cancer cell cycle progression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}
    experimental_model
    Growth-factor stimulation and signaling assays
    exposure
    IGF-I stimulation with lycopene exposure
    limitations
    Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human MCF7 breast cancer cells
    plain_language
    Slower growth was distinguished from simply killing the cells.
    primary_references
    [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    tissue_or_cell_type
    IRS1 phosphorylation, AP-1 and cell cycle

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 702–713

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

    ### lycopene-cell-cycle Lycopene delayed cell-cycle progression without accompanying apoptotic or necrotic cell death in the tested MCF7 cultures. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: Slower growth was distinguished from simply killing the cells. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    Complete structured claim and evidence

  4. Lycopene increased membrane-associated IGF-binding proteins without changing IGF-I receptor number or affinity.

    Lycopene → Membrane-associated IGF-binding proteins in MCF7 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}
    experimental_model
    Growth-factor stimulation and signaling assays
    exposure
    IGF-I stimulation with lycopene exposure
    limitations
    Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human MCF7 breast cancer cells
    plain_language
    The experiment points to altered signal regulation rather than fewer receptors.
    primary_references
    [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    tissue_or_cell_type
    IRS1 phosphorylation, AP-1 and cell cycle

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 689–700

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

    ### lycopene-igfbp Lycopene increased membrane-associated IGF-binding proteins without changing IGF-I receptor number or affinity. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: The experiment points to altered signal regulation rather than fewer receptors. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    Complete structured claim and evidence

  5. Lycopene reduced IGF-I-stimulated IRS1 tyrosine phosphorylation in MCF7 cells.

    Lycopene → IRS1 tyrosine phosphorylation in human MCF7 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}
    experimental_model
    Growth-factor stimulation and signaling assays
    exposure
    IGF-I stimulation with lycopene exposure
    limitations
    Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human MCF7 breast cancer cells
    plain_language
    The growth signal was weaker at an intracellular relay.
    primary_references
    [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    tissue_or_cell_type
    IRS1 phosphorylation, AP-1 and cell cycle

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 663–674

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

    ### lycopene-irs1 Lycopene reduced IGF-I-stimulated IRS1 tyrosine phosphorylation in MCF7 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: The growth signal was weaker at an intracellular relay. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14
    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