Component

KEAP1 C151-sensitive construct in the 2015 cinnamaldehyde study; construct species unresolved from abstract

KEAP1 C151-sensitive construct in the 2015 cinnamaldehyde study; construct species unresolved from abstract. Species, exposure and limitations are retained in each linked claim.

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

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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.

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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. Cinnamaldehyde increased cellular glutathione in the HCT116 NRF2-response study.

    trans-Cinnamaldehyde / cinnamal → HCT116 cellular glutathione content source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"}
    experimental_model
    HCT116 mechanism and AOM/DSS knockout-mouse experiment
    exposure
    Purified cinnamaldehyde cell exposure and dietary supplementation in mice
    limitations
    No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human HCT116 cells; KEAP1 construct species unresolved
    plain_language
    These cells accumulated more glutathione; that does not measure whole-body glutathione supply.
    primary_references
    [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    tissue_or_cell_type
    Colon epithelial cancer cells and experimental inflammatory colon tumors

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 623–634

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HCT116 mechanism and AOM/DSS knockout-mouse experiment · source_derived_draft · unverified_draft

    ### ceylon-nrf2-gsh Cinnamaldehyde increased cellular glutathione in the HCT116 NRF2-response study. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: These cells accumulated more glutathione; that does not measure whole-body glutathione supply. organism: Human HCT116 cells; KEAP1 construct species unresolved tissue_or_cell_type: Colon epithelial cancer cells and experimental inflammatory colon tumors experimental_model: HCT116 mechanism and AOM/DSS knockout-mouse experiment limitations: No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species. exposure: Purified cinnamaldehyde cell exposure and dietary supplementation in mice evidence_span: {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"} [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    Complete structured claim and evidence

  2. Cinnamaldehyde increased NRF2 protein half-life in HCT116 cells.

    trans-Cinnamaldehyde / cinnamal → Nrf2 protein stability source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"}
    experimental_model
    HCT116 mechanism and AOM/DSS knockout-mouse experiment
    exposure
    Purified cinnamaldehyde cell exposure and dietary supplementation in mice
    limitations
    No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human HCT116 cells; KEAP1 construct species unresolved
    plain_language
    NRF2 lasted longer, allowing a stronger defense-gene response.
    primary_references
    [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    tissue_or_cell_type
    Colon epithelial cancer cells and experimental inflammatory colon tumors

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 610–621

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HCT116 mechanism and AOM/DSS knockout-mouse experiment · source_derived_draft · unverified_draft

    ### ceylon-nrf2-stability Cinnamaldehyde increased NRF2 protein half-life in HCT116 cells. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: NRF2 lasted longer, allowing a stronger defense-gene response. organism: Human HCT116 cells; KEAP1 construct species unresolved tissue_or_cell_type: Colon epithelial cancer cells and experimental inflammatory colon tumors experimental_model: HCT116 mechanism and AOM/DSS knockout-mouse experiment limitations: No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species. exposure: Purified cinnamaldehyde cell exposure and dietary supplementation in mice evidence_span: {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"} [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    Complete structured claim and evidence

  3. Cinnamaldehyde blocked NRF2 ubiquitination in HCT116 cells through a KEAP1-C151-dependent mechanism.

    trans-Cinnamaldehyde / cinnamal → KEAP1-dependent Nrf2 ubiquitination source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"}
    experimental_model
    HCT116 mechanism and AOM/DSS knockout-mouse experiment
    exposure
    Purified cinnamaldehyde cell exposure and dietary supplementation in mice
    limitations
    No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human HCT116 cells; KEAP1 construct species unresolved
    plain_language
    The cell marked less NRF2 for disposal.
    primary_references
    [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    tissue_or_cell_type
    Colon epithelial cancer cells and experimental inflammatory colon tumors

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 597–608

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HCT116 mechanism and AOM/DSS knockout-mouse experiment · source_derived_draft · unverified_draft

    ### ceylon-nrf2-ubiquitin Cinnamaldehyde blocked NRF2 ubiquitination in HCT116 cells through a KEAP1-C151-dependent mechanism. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell marked less NRF2 for disposal. organism: Human HCT116 cells; KEAP1 construct species unresolved tissue_or_cell_type: Colon epithelial cancer cells and experimental inflammatory colon tumors experimental_model: HCT116 mechanism and AOM/DSS knockout-mouse experiment limitations: No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species. exposure: Purified cinnamaldehyde cell exposure and dietary supplementation in mice evidence_span: {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"} [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359
    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