Component

Nrf2 nuclear localization

Nrf2 nuclear localization. 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. Sulforaphane increased nuclear localization of stabilized Nrf2 and Nrf2-dependent gene activation.

    Sulforaphane / SFN, stereochemistry specified per study → Nrf2 nuclear localization source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"}
    experimental_model
    KEAP1 mutagenesis and Nrf2 stability/localization assays
    exposure
    Sulforaphane or oxidative stress; C151/C273/C288 variants
    limitations
    Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human KEAP1 constructs in cellular experiments
    plain_language
    The regulator accumulates where it can influence gene expression.
    primary_references
    [sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003
    tissue_or_cell_type
    Ubiquitination, protein turnover and nuclear localization

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 528–539

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KEAP1 mutagenesis and Nrf2 stability/localization assays · source_derived_draft · unverified_draft

    ### sulforaphane-nrf2-nuclear Sulforaphane increased nuclear localization of stabilized Nrf2 and Nrf2-dependent gene activation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The regulator accumulates where it can influence gene expression. organism: Human KEAP1 constructs in cellular experiments tissue_or_cell_type: Ubiquitination, protein turnover and nuclear localization experimental_model: KEAP1 mutagenesis and Nrf2 stability/localization assays limitations: Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans. exposure: Sulforaphane or oxidative stress; C151/C273/C288 variants evidence_span: {"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"} [sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003
    Complete structured claim and evidence

  2. Nrf2 moved from the cytoplasm to the nucleus at 1.5–2 hours after boric-acid treatment of human DU-145 cells.

    Boric acid / orthoboric acid / B(OH)3 → Nrf2 nuclear localization source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}
    experimental_model
    PERK knockout comparison, immunofluorescence and quantitative PCR
    exposure
    10 µM boric acid; 1–6 hour comparisons
    limitations
    Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human
    plain_language
    An antioxidant-response regulator moved to the place where it can influence gene expression.
    primary_references
    [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
    tissue_or_cell_type
    DU-145 prostate cancer cell culture

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 521–532

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

    ### boron-human-nrf2-localization Nrf2 moved from the cytoplasm to the nucleus at 1.5–2 hours after boric-acid treatment of human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: An antioxidant-response regulator moved to the place where it can influence gene expression. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
    Complete structured claim and evidence

  3. Apo-10-prime-lycopenoic acid increased nuclear Nrf2 accumulation in BEAS-2B cells.

    Apo-10-prime-lycopenoic acid → Nrf2 nuclear localization source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/18566994.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534", "start_char": 0, "end_char": 1416, "text_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534"}
    experimental_model
    Metabolite exposure and gene/protein/redox measurements
    exposure
    Time- and dose-dependent apo-10-prime-lycopenoid exposure
    limitations
    Cell-culture metabolite results do not prove oral lycopene reaches equivalent tissue concentrations or prevents human cancer.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human BEAS-2B bronchial epithelial cells
    plain_language
    A defined breakdown product activated the Nrf2-associated response.
    primary_references
    [lycopene-p18566994] Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18566994/ DOI: 10.1002/ijc.23696
    tissue_or_cell_type
    Nucleus, antioxidant enzymes and intracellular glutathione

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 494–505

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolite exposure and gene/protein/redox measurements · source_derived_draft · unverified_draft

    ### lycopene-apo-nrf2 Apo-10-prime-lycopenoic acid increased nuclear Nrf2 accumulation in BEAS-2B cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defined breakdown product activated the Nrf2-associated response. organism: Human BEAS-2B bronchial epithelial cells tissue_or_cell_type: Nucleus, antioxidant enzymes and intracellular glutathione experimental_model: Metabolite exposure and gene/protein/redox measurements limitations: Cell-culture metabolite results do not prove oral lycopene reaches equivalent tissue concentrations or prevents human cancer. exposure: Time- and dose-dependent apo-10-prime-lycopenoid exposure evidence_span: {"source_cache": "artifacts/lycopene-research/18566994.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534", "start_char": 0, "end_char": 1416, "text_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534"} [lycopene-p18566994] Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18566994/ DOI: 10.1002/ijc.23696
    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