Component

MTF1 binding to metal-responsive DNA elements

MTF1 binding to metal-responsive DNA elements; model and exposure are recorded in linked claims.

2 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. Glutathione protected recombinant MTF1 from cadmium-mediated inactivation, allowing zinc-dependent DNA-binding activity in the assay.

    GSH → MTF1 binding to metal-responsive DNA elements source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human metal-regulatory transcription factor 1 / MTF1 (human_protein); Mouse metal-regulatory transcription factor 1 / Mtf1 (mouse_protein); Zinc(II) ion (activating_ion)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/9507026-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ecd19e16b15909d46328c2c5dcd9f9536422db7bb12b9dfd9d91763fafe164bd"}
    experimental_model
    Human and mouse cell extracts and recombinant MTF1
    exposure
    Zinc versus other tested transition metals; DNA-binding assays. Glutathione was 1 mM in the recombinant-protein cadmium challenge; this is an in-vitro assay concentration.
    limitations
    In-vitro metal specificity does not mean all cellular metal responses are mediated by direct MTF1 binding.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens; Mus musculus
    plain_language
    Glutathione helped preserve the zinc-dependent sensor under this chemical stress.
    primary_references
    [zn-sig-9507026] The DNA binding activity of metal response element-binding transcription factor-1 is activated in vivo and in vitro by zinc, but not by other transition metals. (1998). https://pubmed.ncbi.nlm.nih.gov/9507026/ DOI: 10.1074/jbc.273.12.7127
    tissue_or_cell_type
    Cell extracts and recombinant protein

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 887–899

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and mouse cell extracts and recombinant MTF1 · source_derived_draft · unverified_draft

    ### zn-sig-gsh-mtf1-protection Glutathione protected recombinant MTF1 from cadmium-mediated inactivation, allowing zinc-dependent DNA-binding activity in the assay. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione helped preserve the zinc-dependent sensor under this chemical stress. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Cell extracts and recombinant protein experimental_model: Human and mouse cell extracts and recombinant MTF1 limitations: In-vitro metal specificity does not mean all cellular metal responses are mediated by direct MTF1 binding. exposure: Zinc versus other tested transition metals; DNA-binding assays. Glutathione was 1 mM in the recombinant-protein cadmium challenge; this is an in-vitro assay concentration. cross_nutrient: Human metal-regulatory transcription factor 1 / MTF1 (human_protein); Mouse metal-regulatory transcription factor 1 / Mtf1 (mouse_protein); Zinc(II) ion (activating_ion) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/9507026-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ecd19e16b15909d46328c2c5dcd9f9536422db7bb12b9dfd9d91763fafe164bd"} [zn-sig-9507026] The DNA binding activity of metal response element-binding transcription factor-1 is activated in vivo and in vitro by zinc, but not by other transition metals. (1998). https://pubmed.ncbi.nlm.nih.gov/9507026/ DOI: 10.1074/jbc.273.12.7127
    Complete structured claim and evidence

  2. Recombinant human and mouse MTF1 required added zinc for DNA binding; among the tested transition metals, only zinc activated recombinant MTF1 binding.

    Zinc(II) ion → MTF1 binding to metal-responsive DNA elements source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human metal-regulatory transcription factor 1 / MTF1 (human_protein); Mouse metal-regulatory transcription factor 1 / Mtf1 (mouse_protein)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/9507026-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ecd19e16b15909d46328c2c5dcd9f9536422db7bb12b9dfd9d91763fafe164bd"}
    experimental_model
    Human and mouse cell extracts and recombinant MTF1
    exposure
    Zinc versus other tested transition metals; DNA-binding assays.
    limitations
    In-vitro metal specificity does not mean all cellular metal responses are mediated by direct MTF1 binding.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens; Mus musculus
    plain_language
    Zinc acted as a specific input to this metal-responsive transcription factor.
    primary_references
    [zn-sig-9507026] The DNA binding activity of metal response element-binding transcription factor-1 is activated in vivo and in vitro by zinc, but not by other transition metals. (1998). https://pubmed.ncbi.nlm.nih.gov/9507026/ DOI: 10.1074/jbc.273.12.7127
    tissue_or_cell_type
    Cell extracts and recombinant protein

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 873–885

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and mouse cell extracts and recombinant MTF1 · source_derived_draft · unverified_draft

    ### zn-sig-zinc-mtf1-binding Recombinant human and mouse MTF1 required added zinc for DNA binding; among the tested transition metals, only zinc activated recombinant MTF1 binding. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc acted as a specific input to this metal-responsive transcription factor. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Cell extracts and recombinant protein experimental_model: Human and mouse cell extracts and recombinant MTF1 limitations: In-vitro metal specificity does not mean all cellular metal responses are mediated by direct MTF1 binding. exposure: Zinc versus other tested transition metals; DNA-binding assays. cross_nutrient: Human metal-regulatory transcription factor 1 / MTF1 (human_protein); Mouse metal-regulatory transcription factor 1 / Mtf1 (mouse_protein) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/9507026-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ecd19e16b15909d46328c2c5dcd9f9536422db7bb12b9dfd9d91763fafe164bd"} [zn-sig-9507026] The DNA binding activity of metal response element-binding transcription factor-1 is activated in vivo and in vitro by zinc, but not by other transition metals. (1998). https://pubmed.ncbi.nlm.nih.gov/9507026/ DOI: 10.1074/jbc.273.12.7127
    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