Component
Rat pendrin / Slc26a4
Rat orthologue; distinct from human SLC26A4.
3 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 acts on it
Pendrin abundance increased after 24 hours at 1 mM NaI; lower tested concentrations and 48-hour total abundance showed no significant increase.
Experimental context and source evidence
- experimental_model
- Rat thyroid PCCl3 cells; 1 mM NaI unless specified.
- exposure_category
- Experimental iodide excess; normal is the schema category outside deficiency, machinery impairment and biomarker context.
- limitations
- Nonpolarized cells; concurrent changes do not establish pendrin necessity, human protection, or an intake threshold.
- measurement
- Western blot; Figure 1.
- nutrient_topic
- Iodine · Iodine
- primary_references
- Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/
Iodine addendum: iodide excess and cellular export (2026-09-18) · lines 9–11
Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/ · supports · Rat thyroid PCCl3 cells; 1 mM NaI unless specified. · source_derived_draft · unverified_draft
## abundance Pendrin abundance increased after 24 hours at 1 mM NaI; lower tested concentrations and 48-hour total abundance showed no significant increase. Measurement: Western blot; Figure 1.
Complete structured claim and evidenceExcess iodide slowed pendrin loss during cycloheximide treatment, supporting increased protein stability.
Experimental context and source evidence
- experimental_model
- Rat thyroid PCCl3 cells; 1 mM NaI unless specified.
- exposure_category
- Experimental iodide excess; normal is the schema category outside deficiency, machinery impairment and biomarker context.
- limitations
- Nonpolarized cells; concurrent changes do not establish pendrin necessity, human protection, or an intake threshold.
- measurement
- Cycloheximide chase; Figure 4.
- nutrient_topic
- Iodine · Iodine
- primary_references
- Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/
Iodine addendum: iodide excess and cellular export (2026-09-18) · lines 17–19
Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/ · supports · Rat thyroid PCCl3 cells; 1 mM NaI unless specified. · source_derived_draft · unverified_draft
## stability Excess iodide slowed pendrin loss during cycloheximide treatment, supporting increased protein stability. Measurement: Cycloheximide chase; Figure 4.
Complete structured claim and evidenceSurface pendrin increased at 24 and 48 hours by flow cytometry; immunofluorescence also detected an increase at 12 hours.
Experimental context and source evidence
- experimental_model
- Rat thyroid PCCl3 cells; 1 mM NaI unless specified.
- exposure_category
- Experimental iodide excess; normal is the schema category outside deficiency, machinery impairment and biomarker context.
- limitations
- Nonpolarized cells; concurrent changes do not establish pendrin necessity, human protection, or an intake threshold.
- measurement
- Nonpermeabilized staining; Figures 2–3.
- nutrient_topic
- Iodine · Iodine
- primary_references
- Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/
Iodine addendum: iodide excess and cellular export (2026-09-18) · lines 13–15
Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/ · supports · Rat thyroid PCCl3 cells; 1 mM NaI unless specified. · source_derived_draft · unverified_draft
## surface Surface pendrin increased at 24 and 48 hours by flow cytometry; immunofluorescence also detected an increase at 12 hours. Measurement: Nonpermeabilized staining; Figures 2–3.
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.