ArticleNature2025
Transcriptional adaptation upregulates utrophin in Duchenne muscular dystrophy.
Article in Nature, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Zebrafish relatives as models for functional comparative genetics and genomics.Nature reviews. Genetics · 2026Review
- Givinostat enhances antisense oligonucleotide efficacy in theMolecular therapy. Nucleic acids · 2026Article
- Signatures of nonsense-mediated mRNA decay but no evidence for transcriptional adaptation associated with protein-truncating variants in wild yeast diploids.Molecular biology and evolution · 2026Article
- Real-time imaging of transcriptional feedback in nonsense-mediated mRNA decay.Science advances · 2026Article
- Condition-Associated Pattern Extraction and Recovery From Multi-Condition Single-Cell RNA-seq Data With CAPER.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Overlapping expression and co-operative function of the zebrafish pcdh15 paralogs.Communications biology · 2026Article
- Advances in antisense oligonucleotide treatment for cancer.Japanese journal of clinical oncology · 2026Review
- YAP Acts as a Negative Regulator of Mini Utrophin-Based Gene Therapy for Duchenne Muscular Dystrophy in Mdx Mice.International journal of molecular sciences · 2026Article
- RNA-Based Therapies for Treating Monogenic Cardiomyopathies.The Canadian journal of cardiology · 2026Review
- Mechanisms linking cytoplasmic decay of translation-defective mRNA to transcriptional adaptation.Science (New York, N.Y.) · 2026Article
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- PIK3C2A-Related Clinical Phenotype and Cellular Charaterization Linked to Functional SHH Primary Cilia Defect.Clinical genetics · 2025Article
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Exploring Desmin as a Potential Modifier in Duchenne Muscular Dystrophy-Associated Cardiomyopathy.Acta physiologica (Oxford, England) · 2025Article
- Making sense of carbonic anhydrase function in zebrafish using antisense morpholinos.Molecular genetics and genomics : MGG · 2025Review
- Deficient Astrocyte Homeostatic Support Contributes to Brain Impairment in Duchenne Muscular Dystrophy.Neurochemical research · 2025Review
- Study on Leigh syndrome caused byFrontiers in neurologyArticle
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.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a muscle-degenerating disease caused by mutations in the DMD gene, which encodes the dystrophin protein
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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.