Component

Human multidrug resistance-associated protein 1 / ABCC1 / MRP1

Human multidrug resistance-associated protein 1 / ABCC1 / MRP1. 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

What it acts on

  1. MRP1-overexpressing human cells supported rapid export of accumulated sulforaphane, mainly as its glutathione conjugate.

    Human multidrug resistance-associated protein 1 / ABCC1 / MRP1 → Sulforaphane/glutathione-conjugate efflux source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"}
    experimental_model
    Transporter-overexpression and temperature/inhibitor experiments
    exposure
    Sulforaphane loading; ABCC1 or ABCB1 expression
    limitations
    Cancer-cell transport experiments; not a measured clinical drug interaction.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human HL60 leukemia and 8226 myeloma cells
    plain_language
    A transporter can shorten intracellular exposure.
    primary_references
    [sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301
    tissue_or_cell_type
    Intracellular retention and export

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 307–318

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-overexpression and temperature/inhibitor experiments · source_derived_draft · unverified_draft

    ### sulforaphane-abcc1-efflux MRP1-overexpressing human cells supported rapid export of accumulated sulforaphane, mainly as its glutathione conjugate. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter can shorten intracellular exposure. organism: Human HL60 leukemia and 8226 myeloma cells tissue_or_cell_type: Intracellular retention and export experimental_model: Transporter-overexpression and temperature/inhibitor experiments limitations: Cancer-cell transport experiments; not a measured clinical drug interaction. exposure: Sulforaphane loading; ABCC1 or ABCB1 expression evidence_span: {"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"} [sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301
    Complete structured claim and evidence

  2. The sulforaphane-induced Nrf2 increase was less sustained in MRP1-expressing cells, especially with GSTP1 coexpression.

    Human multidrug resistance-associated protein 1 / ABCC1 / MRP1 → Persistence of induced nuclear Nrf2, assay specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"}
    experimental_model
    Transgenic transporter/enzyme comparison
    exposure
    Sulforaphane; GSH depletion control
    limitations
    Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human MCF7 cells with GSTP1 and/or MRP1
    plain_language
    The duration of the response depends partly on how the compound is handled.
    primary_references
    [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
    tissue_or_cell_type
    Intracellular retention, ARE induction and Nrf2 persistence

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1035–1046

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic transporter/enzyme comparison · source_derived_draft · unverified_draft

    ### sulforaphane-mrp-nrf2-duration The sulforaphane-induced Nrf2 increase was less sustained in MRP1-expressing cells, especially with GSTP1 coexpression. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The duration of the response depends partly on how the compound is handled. organism: Human MCF7 cells with GSTP1 and/or MRP1 tissue_or_cell_type: Intracellular retention, ARE induction and Nrf2 persistence experimental_model: Transgenic transporter/enzyme comparison limitations: Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction. exposure: Sulforaphane; GSH depletion control evidence_span: {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"} [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
    Complete structured claim and evidence

  3. MRP1 expression reduced intracellular sulforaphane/conjugate accumulation and attenuated ARE-dependent responses.

    Human multidrug resistance-associated protein 1 / ABCC1 / MRP1 → Intracellular sulforaphane plus glutathione-conjugate accumulation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"}
    experimental_model
    Transgenic transporter/enzyme comparison
    exposure
    Sulforaphane; GSH depletion control
    limitations
    Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human MCF7 cells with GSTP1 and/or MRP1
    plain_language
    Export can counter the retention effect.
    primary_references
    [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
    tissue_or_cell_type
    Intracellular retention, ARE induction and Nrf2 persistence

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1022–1033

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic transporter/enzyme comparison · source_derived_draft · unverified_draft

    ### sulforaphane-mrp-retention MRP1 expression reduced intracellular sulforaphane/conjugate accumulation and attenuated ARE-dependent responses. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Export can counter the retention effect. organism: Human MCF7 cells with GSTP1 and/or MRP1 tissue_or_cell_type: Intracellular retention, ARE induction and Nrf2 persistence experimental_model: Transgenic transporter/enzyme comparison limitations: Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction. exposure: Sulforaphane; GSH depletion control evidence_span: {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"} [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
    Complete structured claim and evidence

  4. MRP1 mediated ATP-dependent GSSG transport; the HeLa-vesicle Km was 93 ± 26 micromolar.

    Human multidrug resistance-associated protein 1 / ABCC1 / MRP1 → ATP-dependent MRP1 glutathione-disulfide transport source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/8670053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3", "start_char": 0, "end_char": 1433, "text_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3"}
    experimental_model
    Membrane-vesicle transport assays
    exposure
    ATP-dependent GSSG uptake into vesicles
    limitations
    Vesicle uptake reflects cellular export; the GSH null result applies specifically to the tested 100 micromolar condition.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human HL60 and HeLa systems
    plain_language
    Oxidized glutathione can be exported instead of recycled locally.
    primary_references
    [glutathione-p8670053] ATP-dependent glutathione disulphide transport mediated by the MRP gene-encoded conjugate export pump. (1996). https://pubmed.ncbi.nlm.nih.gov/8670053/ DOI: 10.1042/bj3140433
    tissue_or_cell_type
    MRP-overexpressing membranes

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 723–734

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Membrane-vesicle transport assays · source_derived_draft · unverified_draft

    ### glutathione-mrp-gssg MRP1 mediated ATP-dependent GSSG transport; the HeLa-vesicle Km was 93 ± 26 micromolar. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized glutathione can be exported instead of recycled locally. organism: Human HL60 and HeLa systems tissue_or_cell_type: MRP-overexpressing membranes experimental_model: Membrane-vesicle transport assays limitations: Vesicle uptake reflects cellular export; the GSH null result applies specifically to the tested 100 micromolar condition. exposure: ATP-dependent GSSG uptake into vesicles evidence_span: {"source_cache": "artifacts/glutathione-research/8670053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3", "start_char": 0, "end_char": 1433, "text_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3"} [glutathione-p8670053] ATP-dependent glutathione disulphide transport mediated by the MRP gene-encoded conjugate export pump. (1996). https://pubmed.ncbi.nlm.nih.gov/8670053/ DOI: 10.1042/bj3140433
    Complete structured claim and evidence

What acts on it

  1. Sulforaphane induced Nrf2-dependent MRP1 expression in CRL-1790 cells.

    Sulforaphane / SFN, stereochemistry specified per study → Human multidrug resistance-associated protein 1 / ABCC1 / MRP1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"}
    experimental_model
    Gene and enzyme-response comparison
    exposure
    Sulforaphane exposure across three cell contexts
    limitations
    Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells
    plain_language
    The response can increase an export transporter as well as enzymes.
    primary_references
    [sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369
    tissue_or_cell_type
    Nrf2 targets and cell defense

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 554–565

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene and enzyme-response comparison · source_derived_draft · unverified_draft

    ### sulforaphane-mrp1-induction Sulforaphane induced Nrf2-dependent MRP1 expression in CRL-1790 cells. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response can increase an export transporter as well as enzymes. organism: Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells tissue_or_cell_type: Nrf2 targets and cell defense experimental_model: Gene and enzyme-response comparison limitations: Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors. exposure: Sulforaphane exposure across three cell contexts evidence_span: {"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"} [sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369
    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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