ArticlePhysiological genomics2011
Gene expression profiling of skeletal muscles treated with a soluble activin type IIB receptor.
Article in Physiological genomics, 2011. 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, 51 citations in OpenAlex.
- Pharmacogenomic Study of Statin-Associated Muscle Symptoms in the ODYSSEY OUTCOMES Trial.Circulation. Genomic and precision medicine · 2022Trial
- Identification of Growth-Related Key Genes Based on Nonlinear Fitting of Weight Growth Curves in Min Pigs.Animals : an open access journal from MDPI · 2026Article
- Identification of Male-Specific Molecular Marker and Development of PCR-Based Genetic Sex Identification Technique in Spotted Knifejaw (Oplegnathus punctatus).Marine biotechnology (New York, N.Y.) · 2022Article
- GCN5 maintains muscle integrity by acetylating YY1 to promote dystrophin expression.The Journal of cell biology · 2022Article
- p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition.Frontiers in physiology · 2021Article
- Muscle NADMolecular metabolism · 2020Article
- Duchenne muscular dystrophy hiPSC-derived myoblast drug screen identifies compounds that ameliorate disease in mdx mice.JCI insight · 2020Article
- Article
- The Hippo Signaling Pathway in the Regulation of Skeletal Muscle Mass and Function.Exercise and sport sciences reviews · 2018Review
- Prevention of chemotherapy-induced cachexia by ACVR2B ligand blocking has different effects on heart and skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2018Article
- Soluble activin receptor type IIB decoy receptor differentially impacts murine osteogenesis imperfecta muscle function.Muscle & nerve · 2018Article
- New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Article
- Systemic blockade of ACVR2B ligands prevents chemotherapy-induced muscle wasting by restoring muscle protein synthesis without affecting oxidative capacity or atrogenes.Scientific reports · 2016Article
- Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Fam65b is important for formation of the HDAC6-dysferlin protein complex during myogenic cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Increasing muscle mass to improve metabolism.Adipocyte · 2013Article
- Muscle wasting and the temporal gene expression pattern in a novel rat intensive care unit model.BMC genomics · 2011Article
- Virtual screening combined with molecular docking for the !identification of new anti-adipogenic compounds.Science progressReview
- Mammalian Mss51 is a skeletal muscle-specific gene modulating cellular metabolism.Journal of neuromuscular diseasesArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Inhibition of the myostatin signaling pathway is emerging as a promising therapeutic means to treat muscle wasting and degenerative disorders. Activin type IIB receptor (ActRIIB) is the putative myostatin receptor, and a soluble activin receptor (ActRIIB-Fc) has been demonstrated to potently inhibit a subset of transforming growth factor (TGF)-β family members including myostatin. To determine reliable and valid biomarkers for ActRIIB-Fc treatment, we assessed gene expression profiles for quadriceps muscles from mice treated with ActRIIB-Fc compared with mice genetically lacking myostatin and control mice. Expression of 134 genes was significantly altered in mice treated with ActRIIB-Fc over a 2-wk period relative to control mice (fold change > 1.5, P < 0.001), whereas the number of significantly altered genes in mice treated for 2 days was 38, demonstrating a time-dependent response to ActRIIB-Fc in overall muscle gene expression. The number of significantly altered genes in Mstn(-/-) mice relative to control mice was substantially higher (360), but for most of these genes the expression levels in the 2-wk treated mice were closer to the levels in the Mstn(-/-) mice than in control mice (P < 10⁻³⁰). Expression levels of 30 selected genes were further validated with quantitative real-time polymerase chain reaction (qPCR), and a correlation of ≥ 0.89 was observed between the fold changes from the microarray analysis and the qPCR analysis. These data suggest that treatment with ActRIIB-Fc results in overlapping but distinct gene expression signatures compared with myostatin genetic mutation. Differentially expressed genes identified in this study can be used as potential biomarkers for ActRIIB-Fc treatment, which is currently in clinical trials as a therapeutic agent for muscle wasting and degenerative disorders.
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