ArticleMolecular and cellular biology2005
Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses 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
54 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Curriculum vitae of CUG binding protein 1 (CELF1) in homeostasis and diseases: a systematic review.Cellular & molecular biology letters · 2024Pooled it
- Pharmacogenomic markers associated with drug-induced QT prolongation: a systematic review.PharmacogenomicsPooled it
- Whole genome association study identifies polymorphisms associated with QT prolongation during iloperidone treatment of schizophrenia.Molecular psychiatry · 2009Trial
- Cytoplasmic RBM20 granules modulate non-RBM20 target splicing through interactions with other splicing factors.Nucleic acids research · 2026Article
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- Integrative transcriptomic profiling links telomere dysfunction to cGAS-STING activation in heart failure signatures in mice and humans.Cardiovascular research · 2026Article
- Alternative mRNA splicing in anthracycline-induced cardiomyopathy - a COG-ALTE03N1 report.Cardio-oncology (London, England) · 2025Article
- Gene expression profiling of human umbilical vein endothelial cells overexpressing CELF2 as diagnostic targets in diabetes-induced erectile dysfunction.Frontiers in molecular biosciences · 2025Article
- RNA-binding proteins in cardiovascular biology and disease: the beat goes on.Nature reviews. Cardiology · 2024Review
- Bruno 1/CELF regulates splicing and cytoskeleton dynamics to ensure correct sarcomere assembly in Drosophila flight muscles.PLoS biology · 2024Article
- RNA binding proteins as mediators of pathological cardiac remodeling.Frontiers in cell and developmental biology · 2024Review
- Epigenetic modifier alpha-ketoglutarate modulates aberrant gene body methylation and hydroxymethylation marks in diabetic heart.Epigenetics & chromatin · 2023Article
- CUGBP1, a crucial factor for heart regeneration in mice.Cell death & disease · 2022Article
- Caenorhabditis elegans ETR-1/CELF has broad effects on the muscle cell transcriptome, including genes that regulate translation and neuroblast migration.BMC genomics · 2022Article
- Alternative Pre-mRNA Splicing of the Mu Opioid Receptor Gene,Biomolecules · 2021Review
- Association of intronic DNA methylation and hydroxymethylation alterations in the epigenetic etiology of dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- Bioinformatic screening for key miRNAs and genes associated with myocardial infarction.FEBS open bio · 2018Article
- Bruno-3 regulates sarcomere component expression and contributes to muscle phenotypes of myotonic dystrophy type 1.Disease models & mechanisms · 2018Article
- Ancient antagonism between CELF and RBFOX families tunes mRNA splicing outcomes.Genome research · 2017Article
- Muscle developmental defects in heterogeneous nuclear Ribonucleoprotein A1 knockout mice.Open biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Members of the CELF family of RNA binding proteins have been implicated in alternative splicing regulation in developing heart. Transgenic mice that express a nuclear dominant-negative CELF protein specifically in the heart (MHC-CELFDelta) develop cardiac hypertrophy and dilated cardiomyopathy with defects in alternative splicing beginning as early as 3 weeks after birth. MHC-CELFDelta mice exhibit extensive cardiac fibrosis, severe cardiac dysfunction, and premature death. Interestingly, the penetrance of the phenotype is greater in females than in males despite similar levels of dominant-negative expression, suggesting that there is sex-specific modulation of splicing activity. The cardiac defects in MHC-CELFdelta mice are directly attributable to reduced levels of CELF activity, as crossing these mice with mice overexpressing CUG-BP1, a wild-type CELF protein, rescues defects in alternative splicing, the severity and incidence of cardiac hypertrophy, and survival. We conclude that CELF protein activity is required for normal alternative splicing in the heart in vivo and that normal CELF-mediated alternative splicing regulation is in turn required for normal cardiac function.
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.