Component

Human NIS p.Thr354Pro

Patient-associated human NIS T354P state; distinct from wild-type protein.

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. Human NIS T354P expressed in COS-7 cells showed markedly reduced iodide uptake compared with normal NIS.

    Human NIS p.Thr354Pro → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells
    exposure
    Patient-derived T354P cDNA expression; uptake concentration not provided in abstract.
    limitations
    The reported patient had goiter and defective accumulation but was essentially euthyroid; do not turn this case into universal hypothyroidism severity.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human protein in African green monkey cells
    plain_language
    A defective NIS protein can limit uptake even when iodide is present.
    primary_references
    [iodine-trans-t354p1997] A homozygous missense mutation of the sodium/iodide symporter gene causing iodide transport defect. (1997). https://pubmed.ncbi.nlm.nih.gov/9398697/ DOI: 10.1210/jcem.82.12.4425
    tissue_or_cell_type
    COS-7 plasma membrane
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 232–243

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells · source_derived_draft · unverified_draft

    ### iodine-trans-t354p-uptake Human NIS T354P expressed in COS-7 cells showed markedly reduced iodide uptake compared with normal NIS. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defective NIS protein can limit uptake even when iodide is present. organism: Human protein in African green monkey cells tissue_or_cell_type: COS-7 plasma membrane experimental_model: Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells limitations: The reported patient had goiter and defective accumulation but was essentially euthyroid; do not turn this case into universal hypothyroidism severity. exposure: Patient-derived T354P cDNA expression; uptake concentration not provided in abstract. cross_nutrient: false [iodine-trans-t354p1997] A homozygous missense mutation of the sodium/iodide symporter gene causing iodide transport defect. (1997). https://pubmed.ncbi.nlm.nih.gov/9398697/ DOI: 10.1210/jcem.82.12.4425
    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