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p(MGI:Igf1) -> bp(GO:"skeletal muscle hypertrophy")
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Results Deacetylase Inhibitors Stimulate Recruitment of Myoblasts into Myotubes To investigate whether HDAC inhibitors favor the recruitment of myoblasts into myotubes or act as hypertrophic agents on preformed myotubes, we exposed C2C12 skeletal muscle cells at different stages of differentiation to the HDAC inhibitor trichostatin A (TSA). Myoblasts exposed to TSA in high-serum medium (growth conditions) and then allowed to differentiate in low-serum medium (differentiation conditions) in the absence of TSA form hypernucleated myotubes with increased cell size (Figure 1A). At the doses employed (50 nM), TSA did not induce apoptosis or signs of cell toxicity (data not shown). IGF-1 promotes hypertrophy of preformed myotubes (Rommel et al., 2001). Therefore, we exposed 2-day-old myotubes to either IGF-1 or TSA. To eliminate the possibility that either IGF-1 or TSA could act on undifferentiated myoblasts present in the myotube culture, arabinoside-C was added to the medium of 2-day-old myotubes for 24 hr before adding IGF-1 or TSA. As expected, IGF-1 induced myotube hypertrophy, while TSA failed to cause any appreciable increase in cell size (Figure 1B).
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Selventa
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2014-07-03T14:30:23.224+02:00
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