Component

SLC26A7 membrane localization

Subcellular position of SLC26A7; apical and basolateral findings are separately scoped.

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 acts on it

  1. Human SLC26A7 Q500Ter expressed in MDCK cells aggregated in the cytosol instead of showing the predominant surface localization of wild-type protein.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings
    exposure
    FLAG-tagged wild-type versus Q500Ter expression; immunofluorescence Fig. 5.
    limitations
    Tagged heterologous expression; localization and current loss are separate observations.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human protein in canine MDCK cells
    plain_language
    This truncation prevents normal transporter placement.
    primary_references
    [iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6
    tissue_or_cell_type
    Cell surface and cytosol
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 349–360

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings · source_derived_draft · unverified_draft

    ### iodine-trans-a7-q500-localization Human SLC26A7 Q500Ter expressed in MDCK cells aggregated in the cytosol instead of showing the predominant surface localization of wild-type protein. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This truncation prevents normal transporter placement. organism: Human protein in canine MDCK cells tissue_or_cell_type: Cell surface and cytosol experimental_model: Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings limitations: Tagged heterologous expression; localization and current loss are separate observations. exposure: FLAG-tagged wild-type versus Q500Ter expression; immunofluorescence Fig. 5. cross_nutrient: false [iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6
    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