ArticleCommunications biology2019
Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7.
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- SLC26A11 is an atypical solute carrier with dual transport-channel function mediating lysosomal sulfate transport.Nature communications · 2026Article
- Structural basis for substrate recognition mechanism of human SLC26A7.Nature communications · 2025Article
- Genetics of primary congenital hypothyroidism: three decades of discoveries and persisting etiological challenges.European thyroid journal · 2025Review
- Thyroid differentiation profile for differentiated thyroid cancer.Endocrine oncology (Bristol, England) · 2025Article
- InvestigatingFrontiers in endocrinology · 2025Article
- Derivation of transplantable human thyroid follicular epithelial cells from induced pluripotent stem cells.Stem cell reports · 2024Article
- CouldDiagnostics (Basel, Switzerland) · 2024Article
- Transcriptomic analysis reveals a critical role for activating GScientific reports · 2024Article
- Deciphering the mystery of CHNG3.Annals of pediatric endocrinology & metabolism · 2024Article
- Late-onset dyshormonogenic goitrous hypothyroidism due to a homozygous mutation of the SLC26A7 gene: a case report.Italian journal of pediatrics · 2024Article
- Chloride/Multiple Anion Exchanger SLC26A Family: Systemic Roles of SLC26A4 in Various Organs.International journal of molecular sciences · 2024Review
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- The Severity of Congenital Hypothyroidism With Gland-In-Situ Predicts Molecular Yield by Targeted Next-Generation Sequencing.The Journal of clinical endocrinology and metabolism · 2023Article
- SLC26 family: a new insight for kidney stone disease.Frontiers in physiology · 2023Review
- Guidelines for Newborn Screening of Congenital Hypothyroidism (2021 Revision).Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2023Article
- Targeted Next-Generation Sequencing of Congenital Hypothyroidism-Causative Genes Reveals Unexpected Thyroglobulin Gene Variants in Patients with Iodide Transport Defect.International journal of molecular sciences · 2022Article
- The iodide transporter Slc26a7 impacts thyroid function more strongly than Slc26a4 in mice.Scientific reports · 2022Article
- MECHANISMS IN ENDOCRINOLOGY: The pathophysiology of transient congenital hypothyroidism.European journal of endocrinology · 2022Review
- Screening of 23 candidate genes by next-generation sequencing of patients with permanent congenital hypothyroidism: novel variants in TG, TSHR, DUOX2, FOXE1, and SLC26A7.Journal of endocrinological investigation · 2022Article
- Intrathyroidal feedforward and feedback network regulating thyroid hormone synthesis and secretion.Frontiers in endocrinology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iodide transport and storage in the thyroid follicles is crucial for thyroid hormone synthesis. Pendrin, the iodide exporter that transports iodide to thyroid follicles, is responsible for Pendred syndrome, a disorder characterized by congenital hypothyroidism and hearing loss. However, thyroid hormone levels are basically normal in patients with Pendred syndrome, indicating the presence of another unknown iodide transporter. Here, we show that SLC26A7 is a novel iodide transporter in the thyroid. We observe that SLC26A7 is specifically expressed in normal thyroid tissues and demonstrate its function in iodide transport. Using whole-exome sequencing, we also find a homozygous nonsense mutation in
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.