ArticleMolecular biology of the cell2016
Staufen1 impairs stress granule formation in skeletal muscle cells from myotonic dystrophy type 1 patients.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 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
- Contribution of the yeast bi-chaperone system in the restoration of the RNA helicase Ded1 and translational activity under severe ethanol stress.The Journal of biological chemistry · 2023Article
- DEHP exposure impairs human skeletal muscle cell proliferation in primary culture conditions: preliminary study.Cytotechnology · 2023Article
- Condensation properties of stress granules and processing bodies are compromised in myotonic dystrophy type 1.Disease models & mechanisms · 2022Article
- Intracellular and intercellular transport of RNA organelles in CXG repeat disorders: The strength of weak ties.Frontiers in molecular biosciences · 2022Review
- High Level of Staufen1 Expression Confers Longer Recurrence Free Survival to Non-Small Cell Lung Cancer Patients by Promoting THBS1 mRNA Degradation.International journal of molecular sciences · 2021Article
- The multifunctional RNA-binding protein Staufen1: an emerging regulator of oncogenesis through its various roles in key cellular events.Cellular and molecular life sciences : CMLS · 2021Review
- Differential regulation of autophagy by STAU1 in alveolar rhabdomyosarcoma and non-transformed skeletal muscle cells.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Temporomandibular Disorders Slow Down the Regeneration Process of Masticatory Muscles: Transcriptomic Analysis.Medicina (Kaunas, Lithuania) · 2021Article
- The dependency of autophagy and ubiquitin proteasome system during skeletal muscle atrophy.Biophysical reviews · 2021Review
- Article
- Cellular Stress in the Pathogenesis of Muscular Disorders-From Cause to Consequence.International journal of molecular sciences · 2020Review
- Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features.Human molecular genetics · 2020Article
- A multipronged approach to understanding the form and function of hStaufen protein.RNA (New York, N.Y.) · 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
- Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles.Human molecular genetics · 2018Article
- RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes.PLoS genetics · 2018Article
- HIV-1 NC-induced stress granule assembly and translation arrest are inhibited by the dsRNA binding protein Staufen1.RNA (New York, N.Y.) · 2018Article
- Novel Roles for Staufen1 in Embryonal and Alveolar Rhabdomyosarcoma via c-myc-dependent and -independent events.Scientific reports · 2017Article
- Staufen1s role as a splicing factor and a disease modifier in Myotonic Dystrophy Type I.Rare diseases (Austin, Tex.) · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Myotonic dystrophy (DM1) is caused by an expansion of CUG repeats (CUG(exp)) in the DMPK mRNA 3'UTR. CUG(exp)-containing mRNAs become toxic to cells by misregulating RNA-binding proteins. Here we investigated the consequence of this RNA toxicity on the cellular stress response. We report that cell stress efficiently triggers formation of stress granules (SGs) in proliferating, quiescent, and differentiated muscle cells, as shown by the appearance of distinct cytoplasmic TIA-1- and DDX3-containing foci. We show that Staufen1 is also dynamically recruited into these granules. Moreover, we discovered that DM1 myoblasts fail to properly form SGs in response to arsenite. This blockage was not observed in DM1 fibroblasts, demonstrating a cell type-specific defect. DM1 myoblasts display increased expression and sequestration of toxic CUG(exp) mRNAs compared with fibroblasts. Of importance, down-regulation of Staufen1 in DM1 myoblasts rescues SG formation. Together our data show that Staufen1 participates in the inhibition of SG formation in DM1 myoblasts. These results reveal that DM1 muscle cells fail to properly respond to stress, thereby likely contributing to the complex pathogenesis of DM1.
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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.