Component

Saccharomyces cerevisiae copper-responsive transcription factor / Mac1

Saccharomyces cerevisiae copper-responsive transcription factor / Mac1. Interpret through the linked study species, preparation, exposure and measured endpoint.

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

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. Deletion of yeast-mac1 increased yeast sensitivity to allicin.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae copper-responsive transcription factor / Mac1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-mac1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-mac1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-mac1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
    plain_language
    Deletion of yeast-mac1 increased yeast sensitivity to allicin.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    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.