Component

KEAP1-dependent Nrf2 ubiquitination

KEAP1-dependent Nrf2 ubiquitination. Species, exposure and limitations are retained in each linked claim.

3 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 acts on it

  1. 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

  2. KEAP1 C151S was markedly resistant to sulforaphane inhibition of its Nrf2-ubiquitination function.

    Human KEAP1 C151S variant → KEAP1-dependent Nrf2 ubiquitination source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"}
    experimental_model
    Cell transfection, coimmunoprecipitation and ubiquitination assays
    exposure
    Sulforaphane or quinone stress; C151S KEAP1 comparison
    limitations
    The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human protein constructs in mammalian cell systems
    plain_language
    An altered sensor can block the response even when the compound is present.
    primary_references
    [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004
    tissue_or_cell_type
    KEAP1-CUL3-RBX1 control of Nrf2
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 502–513

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell transfection, coimmunoprecipitation and ubiquitination assays · source_derived_draft · unverified_draft

    ### sulforaphane-c151s-response KEAP1 C151S was markedly resistant to sulforaphane inhibition of its Nrf2-ubiquitination function. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An altered sensor can block the response even when the compound is present. organism: Human protein constructs in mammalian cell systems tissue_or_cell_type: KEAP1-CUL3-RBX1 control of Nrf2 experimental_model: Cell transfection, coimmunoprecipitation and ubiquitination assays limitations: The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2. exposure: Sulforaphane or quinone stress; C151S KEAP1 comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"} [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004
    Complete structured claim and evidence

  3. Sulforaphane inhibited KEAP1-dependent ubiquitination of Nrf2.

    Sulforaphane / SFN, stereochemistry specified per study → KEAP1-dependent Nrf2 ubiquitination source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"}
    experimental_model
    Cell transfection, coimmunoprecipitation and ubiquitination assays
    exposure
    Sulforaphane or quinone stress; C151S KEAP1 comparison
    limitations
    The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human protein constructs in mammalian cell systems
    plain_language
    Less disposal allows the regulator to persist.
    primary_references
    [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004
    tissue_or_cell_type
    KEAP1-CUL3-RBX1 control of Nrf2

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell transfection, coimmunoprecipitation and ubiquitination assays · source_derived_draft · unverified_draft

    ### sulforaphane-sfn-ubiquitination Sulforaphane inhibited KEAP1-dependent ubiquitination of Nrf2. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less disposal allows the regulator to persist. organism: Human protein constructs in mammalian cell systems tissue_or_cell_type: KEAP1-CUL3-RBX1 control of Nrf2 experimental_model: Cell transfection, coimmunoprecipitation and ubiquitination assays limitations: The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2. exposure: Sulforaphane or quinone stress; C151S KEAP1 comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"} [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004
    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.

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