Component
Human SLC26A7 p.Gln500Ter
Truncated human SLC26A7 from c.1498C>T; associated with congenital goitrous hypothyroidism.
2 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Human SLC26A7 Q500Ter did not produce the wild-type enhancement of iodide-dependent current and iodide-sensitive fluorescence responses in HEK293T cells.
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
- Whole-cell electrophysiology and NaCl-to-NaI solution exchange; Figure 6; iodide-sensitive YFP readout.
- limitations
- These high-ion expression assays do not measure a physiological thyroid efflux rate; direction is determined by the imposed gradients.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens protein and HEK293T cells
- plain_language
- The truncated transporter failed the functional iodide-transport tests.
- 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 plasma membrane
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 362–373
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-current Human SLC26A7 Q500Ter did not produce the wild-type enhancement of iodide-dependent current and iodide-sensitive fluorescence responses in HEK293T cells. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The truncated transporter failed the functional iodide-transport tests. organism: Homo sapiens protein and HEK293T cells tissue_or_cell_type: Cell plasma membrane experimental_model: Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings limitations: These high-ion expression assays do not measure a physiological thyroid efflux rate; direction is determined by the imposed gradients. exposure: Whole-cell electrophysiology and NaCl-to-NaI solution exchange; Figure 6; iodide-sensitive YFP readout. 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 evidenceHuman 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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.