ArticlePLoS genetics2013
Smaug/SAMD4A restores translational activity of CUGBP1 and suppresses CUG-induced myopathy.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- FSHD muscle shows perturbation in fibroadipogenic progenitor cells, mitochondrial function and alternative splicing independently of inflammation.Human molecular genetics · 2024Pooled it
- SAMD4A inhibits abdominal aortic aneurysm development and VSMC phenotypic transformation through targeting KDM2B.Journal of advanced research · 2026Article
- RNA-binding protein SAMD4A targets FGF2 to regulate cardiomyocyte lineage specification from human embryonic stem cells.Stem cell research & therapy · 2025Article
- Curcumin inhibits the proliferation and migration of osteosarcoma by regulating the expression of superZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Deregulations of miR-1 and its target Multiplexin promote dilated cardiomyopathy associated with myotonic dystrophy type 1.EMBO reports · 2023Article
- RNA binding protein SAMD4: current knowledge and future perspectives.Cell & bioscience · 2023Review
- In heart failure reactivation of RNA-binding proteins is associated with the expression of 1,523 fetal-specific isoforms.PLoS computational biology · 2022Article
- hnRNP L is essential for myogenic differentiation and modulates myotonic dystrophy pathologies.Muscle & nerve · 2021Article
- SAMD4 family members suppress human hepatitis B virus by directly binding to the Smaug recognition region of viral RNA.Cellular & molecular immunology · 2021Article
- Regulation of the RNA-binding protein Smaug by the GPCR Smoothened via the kinase Fused.EMBO reports · 2020Article
- circSamd4 represses myogenic transcriptional activity of PUR proteins.Nucleic acids research · 2020Article
- Dissecting Pathogenetic Mechanisms and Therapeutic Strategies inInternational journal of molecular sciences · 2018Review
- Bruno-3 regulates sarcomere component expression and contributes to muscle phenotypes of myotonic dystrophy type 1.Disease models & mechanisms · 2018Article
- Microarray-based detection and expression analysis of new genes associated with drug resistance in ovarian cancer cell lines.Oncotarget · 2017Article
- Review
- RNA-binding protein SAMD4 regulates skeleton development through translational inhibition of Mig6 expression.Cell discovery · 2017Article
- Next generation sequencing profiling identifies miR-574-3p and miR-660-5p as potential novel prognostic markers for breast cancer.BMC genomics · 2015Article
- Model organisms in the fight against muscular dystrophy: lessons from drosophila and Zebrafish.Molecules (Basel, Switzerland) · 2015Review
- Mitochondrial dysfunction reveals the role of mRNA poly(A) tail regulation in oculopharyngeal muscular dystrophy pathogenesis.PLoS genetics · 2015Article
- Mutation of mouse Samd4 causes leanness, myopathy, uncoupled mitochondrial respiration, and dysregulated mTORC1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
We report the identification and characterization of a previously unknown suppressor of myopathy caused by expansion of CUG repeats, the mutation that triggers Myotonic Dystrophy Type 1 (DM1). We screened a collection of genes encoding RNA-binding proteins as candidates to modify DM1 pathogenesis using a well established Drosophila model of the disease. The screen revealed smaug as a powerful modulator of CUG-induced toxicity. Increasing smaug levels prevents muscle wasting and restores muscle function, while reducing its function exacerbates CUG-induced phenotypes. Using human myoblasts, we show physical interactions between human Smaug (SMAUG1/SMAD4A) and CUGBP1. Increased levels of SMAUG1 correct the abnormally high nuclear accumulation of CUGBP1 in myoblasts from DM1 patients. In addition, augmenting SMAUG1 levels leads to a reduction of inactive CUGBP1-eIF2α translational complexes and to a correction of translation of MRG15, a downstream target of CUGBP1. Therefore, Smaug suppresses CUG-mediated muscle wasting at least in part via restoration of translational activity of CUGBP1.
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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.