Component

Human sodium/iodide symporter / SLC5A5

Canonical human NIS protein; transports iodide with sodium.

14 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. Expression of cloned human NIS conferred perchlorate-sensitive iodide uptake on COS-7 cells.

    Human sodium/iodide symporter / SLC5A5 → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human NIS cDNA expressed in COS-7 monkey cells
    exposure
    Transient human NIS cDNA expression; iodide and perchlorate concentrations not reported in the abstract.
    limitations
    Heterologous uptake establishes protein function, not whole-body iodine absorption.
    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
    Human NIS can bring iodide into cells.
    primary_references
    [iodine-trans-human-nis1996] Cloning of the human sodium lodide symporter. (1996). https://pubmed.ncbi.nlm.nih.gov/8806637/ DOI: 10.1006/bbrc.1996.1358
    tissue_or_cell_type
    COS-7 plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 154–165

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NIS cDNA expressed in COS-7 monkey cells · source_derived_draft · unverified_draft

    ### iodine-trans-human-nis-uptake Expression of cloned human NIS conferred perchlorate-sensitive iodide uptake on COS-7 cells. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human NIS can bring iodide into cells. organism: Human protein in African green monkey cells tissue_or_cell_type: COS-7 plasma membrane experimental_model: Human NIS cDNA expressed in COS-7 monkey cells limitations: Heterologous uptake establishes protein function, not whole-body iodine absorption. exposure: Transient human NIS cDNA expression; iodide and perchlorate concentrations not reported in the abstract. cross_nutrient: false [iodine-trans-human-nis1996] Cloning of the human sodium lodide symporter. (1996). https://pubmed.ncbi.nlm.nih.gov/8806637/ DOI: 10.1006/bbrc.1996.1358
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Basolateral iodide reversibly inhibited thiocyanate transport, apparent Ki 9 ± 8 micromolar.

    Iodide ion → Transepithelial airway thiocyanate transport source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    Iodide can compete with another antimicrobial substrate during delivery.
    primary_references
    Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 144–150

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. · source_derived_draft · unverified_draft

    ## ki-air-competition Iodide can compete with another antimicrobial substrate during delivery. Basolateral iodide reversibly inhibited thiocyanate transport, apparent Ki 9 ± 8 micromolar. Model: Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. Limitations: The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect. Evidence location: Primary abstract Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548
    Complete structured claim and evidence

  2. Thiocyanate transport required basolateral sodium and concentrated thiocyanate tenfold apically.

    Sodium ion → Transepithelial airway thiocyanate transport source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    Sodium-dependent delivery supplies the airway defence system.
    primary_references
    Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 152–158

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. · source_derived_draft · unverified_draft

    ## ki-air-sodium Sodium-dependent delivery supplies the airway defence system. Thiocyanate transport required basolateral sodium and concentrated thiocyanate tenfold apically. Model: Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. Limitations: The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect. Evidence location: Primary abstract Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548
    Complete structured claim and evidence

  3. Airway epithelia transported iodide with apparent Km 111 ± 69 micromolar.

    Iodide ion → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    Airway cells can transport iodide.
    primary_references
    Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 136–142

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. · source_derived_draft · unverified_draft

    ## ki-air-transport Airway cells can transport iodide. Airway epithelia transported iodide with apparent Km 111 ± 69 micromolar. Model: Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. Limitations: The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect. Evidence location: Primary abstract Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548
    Complete structured claim and evidence

  4. MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone.

    Human SLC26A7 anion transporter → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings
    exposure
    Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c.
    limitations
    A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human proteins in canine MDCK cells
    plain_language
    SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.
    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
    Polarized epithelial bicameral culture

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 336–347

    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-efflux2019 MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: SLC26A7 increased iodide movement across a polarized cell sheet in this experiment. organism: Human proteins in canine MDCK cells tissue_or_cell_type: Polarized epithelial bicameral culture experimental_model: Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings limitations: A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid. exposure: Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c. 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

  5. Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux.

    Human SLC26A7 anion transporter → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice
    exposure
    NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E.
    limitations
    A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Homo sapiens protein and HEK293 cells
    plain_language
    An earlier cell assay did not detect an iodide export effect from SLC26A7.
    primary_references
    [iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631
    tissue_or_cell_type
    Cultured-cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 375–386

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice · source_derived_draft · unverified_draft

    ### iodine-trans-a7-no-efflux2018 Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An earlier cell assay did not detect an iodide export effect from SLC26A7. organism: Homo sapiens protein and HEK293 cells tissue_or_cell_type: Cultured-cell plasma membrane experimental_model: Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice limitations: A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained. exposure: NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E. cross_nutrient: false [iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631
    Complete structured claim and evidence

  6. Combined loss of AP-1A and AP-1B mu1 subunits reduced trafficking of human NIS to the MDCK cell plasma membrane.

    Canine AP-1A clathrin adaptor complex → NIS delivery to the plasma membrane source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing
    exposure
    Combined mu1A/mu1B depletion; comparison with single-subunit depletion and controls.
    limitations
    The experiment concerns protein delivery; it does not identify a dietary cofactor shortage.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in canine MDCK cells
    plain_language
    Two adaptor systems together support delivery of NIS to the cell surface.
    primary_references
    [iodine-trans-sorting2022] Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes. (2022). https://pubmed.ncbi.nlm.nih.gov/35833460/ DOI: 10.1089/thy.2022.0163
    tissue_or_cell_type
    Epithelial trans-Golgi/recycling-endosome trafficking
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 219–230

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing · source_derived_draft · unverified_draft

    ### iodine-trans-ap1-double-delivery Combined loss of AP-1A and AP-1B mu1 subunits reduced trafficking of human NIS to the MDCK cell plasma membrane. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two adaptor systems together support delivery of NIS to the cell surface. organism: Human NIS in canine MDCK cells tissue_or_cell_type: Epithelial trans-Golgi/recycling-endosome trafficking experimental_model: Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing limitations: The experiment concerns protein delivery; it does not identify a dietary cofactor shortage. exposure: Combined mu1A/mu1B depletion; comparison with single-subunit depletion and controls. cross_nutrient: false [iodine-trans-sorting2022] Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes. (2022). https://pubmed.ncbi.nlm.nih.gov/35833460/ DOI: 10.1089/thy.2022.0163
    Complete structured claim and evidence

  7. Depletion of the AP-1B mu1B subunit in polarized MDCK cells caused expressed human NIS to be missorted toward the apical membrane while retaining transport function.

    Canine AP-1B clathrin adaptor complex → NIS basolateral membrane targeting source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing
    exposure
    AP-1B mu1B silencing compared with control MDCK-hNIS cells.
    limitations
    Engineered epithelial model; apical uptake does not establish useful blood-to-thyroid delivery in vivo.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in canine MDCK cells
    plain_language
    Correct membrane placement depends on the cell’s sorting machinery.
    primary_references
    [iodine-trans-sorting2022] Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes. (2022). https://pubmed.ncbi.nlm.nih.gov/35833460/ DOI: 10.1089/thy.2022.0163
    tissue_or_cell_type
    Polarized epithelial plasma membrane
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 206–217

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing · source_derived_draft · unverified_draft

    ### iodine-trans-ap1b-polarity Depletion of the AP-1B mu1B subunit in polarized MDCK cells caused expressed human NIS to be missorted toward the apical membrane while retaining transport function. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correct membrane placement depends on the cell’s sorting machinery. organism: Human NIS in canine MDCK cells tissue_or_cell_type: Polarized epithelial plasma membrane experimental_model: Human NIS expressed in canine MDCK epithelial cells with AP-1 adaptor subunit silencing limitations: Engineered epithelial model; apical uptake does not establish useful blood-to-thyroid delivery in vivo. exposure: AP-1B mu1B silencing compared with control MDCK-hNIS cells. cross_nutrient: false [iodine-trans-sorting2022] Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes. (2022). https://pubmed.ncbi.nlm.nih.gov/35833460/ DOI: 10.1089/thy.2022.0163
    Complete structured claim and evidence

  8. Mixtures of perchlorate, thiocyanate and nitrate inhibited human NIS-mediated iodide uptake consistently with an additive common competitive model, without evidence of synergism.

    Perchlorate ion → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
    exposure
    Joint Hill-equation fit; perchlorate molar potency was 15 times thiocyanate and 240 times nitrate.
    limitations
    Relative potencies and lack of synergy are assay-specific; they do not predict individual human thyroid outcomes from environmental concentrations.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in hamster CHO cells
    plain_language
    These competitors combined approximately additively in the tested cell system.
    primary_references
    [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    tissue_or_cell_type
    Cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 440–451

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft

    ### iodine-trans-inhibitor-additivity Mixtures of perchlorate, thiocyanate and nitrate inhibited human NIS-mediated iodide uptake consistently with an additive common competitive model, without evidence of synergism. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: These competitors combined approximately additively in the tested cell system. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: Relative potencies and lack of synergy are assay-specific; they do not predict individual human thyroid outcomes from environmental concentrations. exposure: Joint Hill-equation fit; perchlorate molar potency was 15 times thiocyanate and 240 times nitrate. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    Complete structured claim and evidence

  9. Nitrate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Nitrate ion → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
    exposure
    Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
    limitations
    In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in hamster CHO cells
    plain_language
    A competing anion reduced iodide entry through human NIS in a cell assay.
    primary_references
    [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    tissue_or_cell_type
    Cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 427–438

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft

    ### iodine-trans-nitrate-inhibits Nitrate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    Complete structured claim and evidence

  10. Human pendrin expression supported iodide efflux in COS-7 and CHO mammalian-cell transport experiments.

    Human pendrin / SLC26A4 → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison
    exposure
    Pendrin/NIS transfection; concentrations not provided in abstract.
    limitations
    Expression-cell data do not establish exclusive thyroid efflux control or transport specificity in every tissue.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human protein in monkey COS-7 and hamster CHO cells
    plain_language
    Pendrin can let iodide leave cells.
    primary_references
    [iodine-trans-pendrin-efflux2002] Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. (2002). https://pubmed.ncbi.nlm.nih.gov/12107249/ DOI: 10.1210/jcem.87.7.8679
    tissue_or_cell_type
    Cultured-cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 297–308

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison · source_derived_draft · unverified_draft

    ### iodine-trans-pendrin-efflux Human pendrin expression supported iodide efflux in COS-7 and CHO mammalian-cell transport experiments. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pendrin can let iodide leave cells. organism: Human protein in monkey COS-7 and hamster CHO cells tissue_or_cell_type: Cultured-cell plasma membrane experimental_model: Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison limitations: Expression-cell data do not establish exclusive thyroid efflux control or transport specificity in every tissue. exposure: Pendrin/NIS transfection; concentrations not provided in abstract. cross_nutrient: false [iodine-trans-pendrin-efflux2002] Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. (2002). https://pubmed.ncbi.nlm.nih.gov/12107249/ DOI: 10.1210/jcem.87.7.8679
    Complete structured claim and evidence

  11. Perchlorate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Perchlorate ion → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
    exposure
    Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
    limitations
    In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in hamster CHO cells
    plain_language
    A competing anion reduced iodide entry through human NIS in a cell assay.
    primary_references
    [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    tissue_or_cell_type
    Cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 401–412

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft

    ### iodine-trans-perchlorate-inhibits Perchlorate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    Complete structured claim and evidence

  12. 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

  13. Thiocyanate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Thiocyanate ion → Cellular iodide uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
    exposure
    Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
    limitations
    In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human NIS in hamster CHO cells
    plain_language
    A competing anion reduced iodide entry through human NIS in a cell assay.
    primary_references
    [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    tissue_or_cell_type
    Cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 414–425

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft

    ### iodine-trans-thiocyanate-inhibits Thiocyanate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
    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