ArticleNucleic acids research2016
Conservation of context-dependent splicing activity in distant Muscleblind homologs.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Predicting circRNA subcellular localization by fusing circRNA sequence and network information.Scientific reports · 2026Article
- The role of genetic variation in shaping phenotypic responses to diet in aging Drosophila melanogaster.Heredity · 2025Article
- Myotonic dystrophy type 1: clinical diversity, molecular insights and therapeutic perspectives.Nature reviews. Neurology · 2025Review
- Functions of the Muscleblind-like protein family and their role in disease.Cell communication and signaling : CCS · 2025Review
- MBNL overexpression rescues cardiac phenotypes in a myotonic dystrophy type 1 heart mouse model.The Journal of clinical investigation · 2025Article
- MBL-1/Muscleblind regulates neuronal differentiation and controls the splicing of a terminal selector in Caenorhabditis elegans.PLoS genetics · 2024Article
- Muscleblind-like proteins use modular domains to localize RNAs by riding kinesins and docking to membranes.Nature communications · 2023Article
- Alternative splicing mediates the compensatory upregulation of MBNL2 upon MBNL1 loss-of-function.Nucleic acids research · 2023Article
- Zebrafish mbnl mutants model physical and molecular phenotypes of myotonic dystrophy.Disease models & mechanisms · 2021Article
- An engineered RNA binding protein with improved splicing regulation.Nucleic acids research · 2018Article
- Structural Basis for Interaction of the Tandem Zinc Finger Domains of Human Muscleblind with Cognate RNA from Human Cardiac Troponin T.Biochemistry · 2017Article
- Repeat-associated RNA structure and aberrant splicing.Biochimica et biophysica acta. Gene regulatory mechanismsReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The Muscleblind (MBL) protein family is a deeply conserved family of RNA binding proteins that regulate alternative splicing, alternative polyadenylation, RNA stability and RNA localization. Their inactivation due to sequestration by expanded CUG repeats causes symptoms in the neuromuscular disease myotonic dystrophy. MBL zinc fingers are the most highly conserved portion of these proteins, and directly interact with RNA. We identified putative MBL homologs in Ciona intestinalis and Trichoplax adhaerens, and investigated their ability, as well as that of MBL homologs from human/mouse, fly and worm, to regulate alternative splicing. We found that all homologs can regulate alternative splicing in mouse cells, with some regulating over 100 events. The cis-elements through which each homolog exerts its splicing activities are likely to be highly similar to mammalian Muscleblind-like proteins (MBNLs), as suggested by motif analyses and the ability of expanded CUG repeats to inactivate homolog-mediated splicing. While regulation of specific target exons by MBL/MBNL has not been broadly conserved across these species, genes enriched for MBL/MBNL binding sites in their introns may play roles in cell adhesion, ion transport and axon guidance, among other biological pathways, suggesting a specific, conserved role for these proteins across a broad range of metazoan species.
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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.