ReviewFrontiers in pharmacology2018
Role of the SLC26A9 Chloride Channel as Disease Modifier and Potential Therapeutic Target in Cystic Fibrosis.
Review in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Impact of Gene Modifiers on Cystic Fibrosis Phenotypic Profiles: A Systematic Review.Human mutation · 2024Pooled it
- Host-Pathogen Interactions in Cystic Fibrosis Lung Disease: Adaptation, Persistence, and Clinical Implications ofPathogens (Basel, Switzerland) · 2026Review
- Pancreatitis: correcting CFTR expression and function as a promising effective treatment.Frontiers in physiology · 2026Review
- Reflection confocal microscopy for quantitative assessment of airway surface layer dysregulation and pharmacological rescue in cystic fibrosis under near-physiological conditions.Scientific reports · 2025Article
- Lack of SLC26A9-mediated chloride secretion causes mucus plugging and severe respiratory distress in neonatal mice.JCI insight · 2025Article
- Integrated multi-sample transcriptomic analysis of COVID-19 patients against controls using a bioinformatics pipeline.Scientific reports · 2025Article
- Progress of personalized medicine of cystic fibrosis in the times of efficient CFTR modulators.Molecular and cellular pediatrics · 2025Review
- SLC26A9 in triple-negative breast cancer stem cells: a network pharmacology and molecular modeling study.Frontiers in bioengineering and biotechnology · 2025Review
- The role of the STAS domain in SLC26A9 for chloride ion transporter function.Biophysical journal · 2024Article
- Putting bicarbonate on the spot: pharmacological insights for CFTR correction in the airway epithelium.Frontiers in pharmacology · 2023Article
- Measuring cystic fibrosis drug responses in organoids derived from 2D differentiated nasal epithelia.Life science alliance · 2022Article
- Genetic evidence supports the development of SLC26A9 targeting therapies for the treatment of lung disease.NPJ genomic medicine · 2022Article
- General Features and Novel Gene Signatures That Identify Epstein-Barr Virus-Associated Epithelial Cancers.Cancers · 2021Article
- SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain.The Biochemical journal · 2021Article
- Recurring exposure to low humidity induces transcriptional and protein level changes in the vocal folds of rabbits.Scientific reports · 2021Article
- Synergy in Cystic Fibrosis Therapies: Targeting SLC26A9.International journal of molecular sciences · 2021Article
- Treatment of Pulmonary Disease of Cystic Fibrosis: A Comprehensive Review.Antibiotics (Basel, Switzerland) · 2021Review
- Cystic Fibrosis-Related Diabetes (CFRD): Overview of Associated Genetic Factors.Diagnostics (Basel, Switzerland) · 2021Review
- Pharmacological Modulation of Ion Channels for the Treatment of Cystic Fibrosis.Journal of experimental pharmacology · 2021Review
- Cystic Fibrosis: Emergence of Highly Effective Targeted Therapeutics and Potential Clinical Implications.American journal of respiratory and critical care medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The solute carrier family 26, member 9 (SLC26A9) is an epithelial chloride channel that is expressed in several organs affected in patients with cystic fibrosis (CF) including the lungs, the pancreas, and the intestine. Emerging evidence suggests SLC26A9 as a modulator of wild-type and mutant CFTR function, and as a potential alternative target to circumvent the basic ion transport defect caused by deficient CFTR-mediated chloride transport in CF. In this review, we summarize
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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.