ArticleHuman molecular genetics2013
Progressive impairment of muscle regeneration in muscleblind-like 3 isoform knockout mice.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 70 citations in OpenAlex.
- Aberrant neuronal differentiation and splicing defects in Congenital Myotonic Dystrophy (DM1) iPSC models.bioRxiv : the preprint server for biology · 2026Article
- MBNL proteins in health, disease, and therapeutic applications.Nucleic acids research · 2026Review
- Cardiac Involvement in Myotonic Dystrophy Type 1: Mechanisms, Clinical Perspectives, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Transcriptome alterations underlying metabolic dysfunction and liver disease in myotonic dystrophy type 1.Human molecular genetics · 2025Article
- MBNL overexpression rescues cardiac phenotypes in a myotonic dystrophy type 1 heart mouse model.The Journal of clinical investigation · 2025Article
- AntimiR treatment corrects myotonic dystrophy primary cell defects across several CTG repeat expansions with a dual mechanism of action.Science advances · 2024Article
- Studying the Effect of MBNL1 and MBNL2 Loss in Skeletal Muscle Regeneration.International journal of molecular sciences · 2024Article
- Peptide-conjugated antimiRs improve myotonic dystrophy type 1 phenotypes by promoting endogenous MBNL1 expression.Molecular therapy. Nucleic acids · 2023Article
- Muscleblind-like proteins use modular domains to localize RNAs by riding kinesins and docking to membranes.Nature communications · 2023Article
- Cytoplasmic forces functionally reorganize nuclear condensates in oocytes.Nature communications · 2022Article
- Molecular Therapies for Myotonic Dystrophy Type 1: From Small Drugs to Gene Editing.International journal of molecular sciences · 2022Review
- The X-linked splicing regulator MBNL3 has been co-opted to restrict placental growth in eutherians.PLoS biology · 2022Article
- A comprehensive atlas of fetal splicing patterns in the brain of adult myotonic dystrophy type 1 patients.NAR genomics and bioinformatics · 2022Article
- CRISPR gene editing in pluripotent stem cells reveals the function of MBNL proteins during human in vitro myogenesis.Human molecular genetics · 2021Article
- Zebrafish mbnl mutants model physical and molecular phenotypes of myotonic dystrophy.Disease models & mechanisms · 2021Article
- The sustained expression of Cas9 targeting toxic RNAs reverses disease phenotypes in mouse models of myotonic dystrophy type 1.Nature biomedical engineering · 2021Article
- RNA-Binding Proteins in the Post-transcriptional Control of Skeletal Muscle Development, Regeneration and Disease.Frontiers in cell and developmental biology · 2021Review
- The zinc finger domains in U2AF26 and U2AF35 have diverse functionalities including a role in controlling translation.RNA biology · 2020Article
- Loss of MBNL1 induces RNA misprocessing in the thymus and peripheral blood.Nature communications · 2020Article
- HNRNPA1-induced spliceopathy in a transgenic mouse model of myotonic dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The muscleblind-like (MBNL) genes encode alternative splicing factors that are essential for the postnatal development of multiple tissues, and the inhibition of MBNL activity by toxic C(C)UG repeat RNAs is a major pathogenic feature of the neuromuscular disease myotonic dystrophy. While MBNL1 controls fetal-to-adult splicing transitions in muscle and MBNL2 serves a similar role in the brain, the function of MBNL3 in vivo is unknown. Here, we report that mouse Mbnl3, which encodes protein isoforms that differ in the number of tandem zinc-finger RNA-binding motifs and subcellular localization, is expressed primarily during embryonic development but also transiently during injury-induced adult skeletal muscle regeneration. Mbnl3 expression is required for normal C2C12 myogenic differentiation and high-throughput sequencing combined with cross-linking/immunoprecipitation analysis indicates that Mbnl3 binds preferentially to the 3' untranslated regions of genes implicated in cell growth and proliferation. In addition, Mbnl3ΔE2 isoform knockout mice, which fail to express the major Mbnl3 nuclear isoform, show age-dependent delays in injury-induced muscle regeneration and impaired muscle function. These results suggest that Mbnl3 inhibition by toxic RNA expression may be a contributing factor to the progressive skeletal muscle weakness and wasting characteristic of myotonic dystrophy.
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.