ArticleMolecular and cellular biology2003
S100B inhibits myogenic differentiation and myotube formation in a RAGE-independent manner.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 78 citations in OpenAlex.
- S100B actions on glial and neuronal cells in the developing brain: an overview.Frontiers in neuroscience · 2024Review
- PGC-1α Agonist Rescues Doxorubicin-Induced Cardiomyopathy by Mitigating the Oxidative Stress and Necroptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Satellite Cell Expression of RAGE (Receptor for Advanced Glycation end Products) Is Important for Collateral Vessel Formation.Journal of the American Heart Association · 2021Article
- Article
- Functional skeletal muscle constructs from transdifferentiated human fibroblasts.Scientific reports · 2020Article
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- Cellular and molecular mechanisms of sarcopenia: the S100B perspective.Journal of cachexia, sarcopenia and muscle · 2018Review
- GSK3β inhibitor promotes myelination and mitigates muscle atrophy after peripheral nerve injury.Neural regeneration research · 2018Article
- Levels of S100B protein drive the reparative process in acute muscle injury and muscular dystrophy.Scientific reports · 2017Article
- Article
- Opposite roles of myocardin and atrogin-1 in L6 myoblast differentiation.Journal of cellular physiology · 2013Article
- S100B protein in tissue development, repair and regeneration.World journal of biological chemistry · 2013Article
- Gene expression profiling identifies molecular pathways associated with collagen VI deficiency and provides novel therapeutic targets.PloS one · 2013Article
- Functions of S100 proteins.Current molecular medicine · 2013Review
- An image analysis method for the precise selection and quantitation of fluorescently labeled cellular constituents: application to the measurement of human muscle cells in culture.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- S100 proteins in cartilage: role in arthritis.Biochimica et biophysica acta · 2012Review
- Article
- Human muscle satellite cells show age-related differential expression of S100B protein and RAGE.Age (Dordrecht, Netherlands) · 2011Article
- Article
- The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.PLoS pathogens · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
S100B is a Ca(2+)-modulated protein of the EF-hand type with both intracellular and extracellular roles. S100B, which is most abundant in the brain, has been shown to exert trophic and toxic effects on neurons depending on the concentration attained in the extracellular space. S100B is also found in normal serum, and its serum concentration increases in several nervous and nonnervous pathological conditions, suggesting that S100B-expressing cells outside the brain might release the protein and S100B might exert effects on nonnervous cells. We show here that at picomolar to nanomolar levels, S100B inhibits myogenic differentiation of rat L6 myoblasts via inactivation of p38 kinase with resulting decrease in the expression of the myogenic differentiation markers, myogenin, muscle creatine kinase, and myosin heavy chain, and reduction of myotube formation. Although myoblasts express the multiligand receptor RAGE, which has been shown to transduce S100B effects on neurons, S100B produces identical effects on myoblasts overexpressing either full-length RAGE or RAGE lacking the transducing domain. This suggests that S100B affects myoblasts by interacting with another receptor and that RAGE is not the only receptor for S100B. Our data suggest that S100B might participate in the regulation of muscle development and regeneration by inhibiting crucial steps of the myogenic program in a RAGE-independent manner.
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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.