ArticleMolecular medicine (Cambridge, Mass.)2016
Reduction of Cellular Expression Levels Is a Common Feature of Functionally Affected Pendrin (SLC26A4) Protein Variants.
Article in Molecular medicine (Cambridge, Mass.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Task force Guideline of Brazilian Society of Otology ‒ hearing loss in children - Part I ‒ Evaluation.Brazilian journal of otorhinolaryngologyGuideline
- The ZBTB16/CUL3/ROC1 ubiquitin ligase drives the degradation of pathogenic pendrin (SLC26A4) protein variants.Journal of biomedical science · 2026Article
- Clinical and genetic heterogeneity of syndromic hearing loss and its non-syndromic hearing loss mimics.Molecular medicine (Cambridge, Mass.) · 2026Article
- Genetic heterogeneity in patients with enlarged vestibular aqueduct and Pendred syndrome.Molecular medicine (Cambridge, Mass.) · 2025Article
- Inhibitors of the ubiquitin‑proteasome system rescue cellular levels and ion transport function of pathogenic pendrin (SLC26A4) protein variants.International journal of molecular medicine · 2025Article
- Novel genetic determinants contribute to hearing loss in a central European cohort with enlarged vestibular aqueduct.Molecular medicine (Cambridge, Mass.) · 2025Article
- SLC26A4-AP-2 mu2 interaction regulates SLC26A4 plasma membrane abundance in the endolymphatic sac.Science advances · 2024Article
- Functional Studies of Deafness-Associated Pendrin and Prestin Variants.International journal of molecular sciences · 2024Article
- Asymmetric pendrin homodimer reveals its molecular mechanism as anion exchanger.Nature communications · 2023Article
- Molecular Features of SLC26A4 Common Variant p.L117F.Journal of clinical medicine · 2022Article
- Atypical Presentation of Enlarged Vestibular Aqueducts Caused byChildren (Basel, Switzerland) · 2022Article
- Novel POU3F4 variants identified in patients with inner ear malformations exhibit aberrant cellular distribution and lack ofFrontiers in molecular neuroscience · 2022Article
- Genetic Determinants of Non-Syndromic Enlarged Vestibular Aqueduct: A Review.Audiology research · 2021Review
- Systematic quantification of the anion transport function of pendrin (SLC26A4) and its disease-associated variants.Human mutation · 2020Article
- Contribution of SLC26A4 to the molecular diagnosis of nonsyndromic prelingual sensorineural hearing loss in a Brazilian cohort.BMC research notes · 2018Article
- Functional Testing of SLC26A4 Variants-Clinical and Molecular Analysis of a Cohort with Enlarged Vestibular Aqueduct from Austria.International journal of molecular sciences · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sequence alterations in the pendrin gene (
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.