ArticleNucleic acids research2012
New function for the RNA helicase p68/DDX5 as a modifier of MBNL1 activity on expanded CUG repeats.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 75 citations in OpenAlex.
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Multiple Defects in Muscle Regeneration in the HSALR Mouse Model of RNA Toxicity.International journal of molecular sciences · 2025Article
- Expression levels of core spliceosomal proteins modulate the MBNL-mediated spliceopathy in DM1.Human molecular genetics · 2024Article
- Identification of protein aggregates in the aging vertebrate brain with prion-like and phase-separation properties.Cell reports · 2024Article
- Deciphering novel TCF4-driven mechanisms underlying a common triplet repeat expansion-mediated disease.PLoS genetics · 2024Article
- Modulatory role of RNA helicases in MBNL-dependent alternative splicing regulation.Cellular and molecular life sciences : CMLS · 2023Article
- Cellular functions of eukaryotic RNA helicases and their links to human diseases.Nature reviews. Molecular cell biology · 2023Review
- Cognate RNA-Binding Modes by the Alternative-Splicing Regulator MBNL1 Inferred from Molecular Dynamics.International journal of molecular sciences · 2022Article
- DEAD-Box RNA Helicases DDX3X and DDX5 as Oncogenes or Oncosuppressors: A Network Perspective.Cancers · 2022Review
- Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats.Nature biomedical engineering · 2022Article
- Transcriptome changes in DM1 patients' tissues are governed by the RNA interference pathway.Frontiers in molecular biosciences · 2022Article
- RNA Helicases in Microsatellite Repeat Expansion Disorders and Neurodegeneration.Frontiers in genetics · 2022Review
- microRNA-mRNA Profile of Skeletal Muscle Differentiation and Relevance to Congenital Myotonic Dystrophy.International journal of molecular sciences · 2021Article
- RNA-Binding Proteins in the Post-transcriptional Control of Skeletal Muscle Development, Regeneration and Disease.Frontiers in cell and developmental biology · 2021Review
- Overlapping mechanisms of lncRNA and expanded microsatellite RNA.Wiley interdisciplinary reviews. RNA · 2021Review
- Review
- Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features.Human molecular genetics · 2020Article
- Intrinsic Regulatory Role of RNA Structural Arrangement in Alternative Splicing Control.International journal of molecular sciences · 2020Review
- Intragenic recruitment of NF-κB drives splicing modifications upon activation by the oncogene Tax of HTLV-1.Nature communications · 2020Article
- Correction of RNA-Binding Protein CUGBP1 and GSK3β Signaling as Therapeutic Approach for Congenital and Adult Myotonic Dystrophy Type 1.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic Dystrophy type I (DM1) is caused by an abnormal expansion of CTG triplets in the 3' UTR of the dystrophia myotonica protein kinase (DMPK) gene, leading to the aggregation of the mutant transcript in nuclear RNA foci. The expanded mutant transcript promotes the sequestration of the MBNL1 splicing factor, resulting in the misregulation of a subset of alternative splicing events. In this study, we identify the DEAD-box RNA helicase p68 (DDX5) in complexes assembled onto in vitro-transcribed CUG repeats. We showed that p68 colocalized with RNA foci in cells expressing the 3'UTR of the DMPK gene containing expanded CTG repeats. We found that p68 increased MBNL1 binding onto pathological repeats and the stem-loop structure regulatory element within the cardiac Troponin T (TNNT2) pre-mRNA, splicing of which is misregulated in DM1. Mutations in the helicase core of p68 prevented both the stimulatory effect of the protein on MBNL1 binding and the colocalization of p68 with CUG repeats, suggesting that remodeling of RNA secondary structure by p68 facilitates MBNL1 binding. We also found that the competence of p68 for regulating TNNT2 exon 5 inclusion depended on the integrity of MBNL1 binding sites. We propose that p68 acts as a modifier of MBNL1 activity on splicing targets and pathogenic RNA.
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