ArticleAmerican journal of physiology. Cell physiology2009
IGF-I activates the mouse type IIb myosin heavy chain gene.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
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- Active GSK3β and an intact β-catenin TCF complex are essential for the differentiation of human myogenic progenitor cells.Scientific reports · 2017Article
- Transiently active Wnt/β-catenin signaling is not required but must be silenced for stem cell function during muscle regeneration.Stem cell reports · 2014Article
- Shaping organs by a wingless-int/Notch/nonmuscle myosin module which orients feather bud elongation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- How to make rapid eye movements "rapid": the role of growth factors for muscle contractile properties.Pflugers Archiv : European journal of physiology · 2011Article
- Segregation of myoblast fusion and muscle-specific gene expression by distinct ligand-dependent inactivation of GSK-3β.Cellular and molecular life sciences : CMLS · 2011Article
- Connective tissue fibroblasts and Tcf4 regulate myogenesis.Development (Cambridge, England) · 2011Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
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Abstract
IGF-I increases skeletal muscle mass, but whether IGF-I increases type IIb myosin heavy chain (MyHC) transcriptional activity is not known. C2C12 myotubes were cultured with or without IGF-I to determine whether IGF-I increases type IIb MyHC promoter activity, and if so, what region of the promoter might IGF-I signaling regulate. At differentiation days 3 and 4, IGF-I increased type IIb MyHC mRNA and mouse 3.0-kb type IIb MyHC promoter activity. Deletion construct studies identified a potential IGF-I-responsive region between 1.25 and 1.2 kb of the type IIb MyHC promoter, which contained an exact 6-bp T-cell factor/lymphoid enhancer factor (Tcf/Lef) binding site at position -1206 to -1201. Site-specific mutation of the putative Tcf/Lef binding site reduced IGF-I-induced 1.3-kb type IIb MyHC promoter activity. To identify potential IGF-I signaling molecules, the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY-294002 were both found to markedly attenuate IGF-I activation of the 1.3-kb type IIb MyHC promoter. Downstream signaling of IGF-I can phosphorylate and inactivate GSK-3beta, thereby enhancing beta-catenin protein. The GSK-3beta inhibitor, LiCl, dramatically enhanced IGF-I induction of the 1.3-kb type IIb MyHC promoter, and constitutively active GSK-3beta attenuated IGF-I-induced 1.3-kb type IIb MyHC promoter activity. Finally, IGF-I increased nuclear beta-catenin protein, and small interfering RNA knockdown of beta-catenin attenuated IGF-I-induced 1.3-kb type IIb MyHC promoter activity and type IIb MyHC mRNA. In summary, IGF-I stimulation of C2C12 myotubes increases mouse type IIb MyHC promoter activity, likely through signaling of PI3K, GSK-3beta, beta-catenin, and a Tcf/Lef binding site at -1,206 to -1,201 bp in the promoter.
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