Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways

By C. Rommel, S. Bodine, B. A. Clarke, Roni Rossman, L. Nuñez, T. Stitt, G. Yancopoulos, D. Glass. Nature Cell Biology, 2001

1,642 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f3a8b29a2005cf2d357a85785879305d16c55ab0

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In Genetics

1. J. Hawley
2. David M. Sabatini
3. A. Goldberg
4. Vernon G. Coffey
5. D. Glass
6. R. A. Saxton
7. J. Blenis
8. P. Russell

In Molecular Biology

1. David M. Sabatini
2. A. Goldberg
3. D. Glass
4. R. A. Saxton
5. M. Sandri
6. J. Blenis
7. N. Hay
8. J. Hawley

Citations in the corpus

• An official American Thoracic Society/European Respiratory Society statement: update on limb muscle dysfunction in chronic obstructive pulmonary disease. (2014, background): “After being phosphorylated itself, AKT phosphorylates several proteins whose activation (mammalian target of rapamycin [mTOR] [128] and 70-kD ribosomal S6 protein [p70S6] kinase) or inhibition (glycogen synthase kinase-3b [GSK3b]) will enhance protein synthesis (116, 118, 128).”
• The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. (2004, background): “, 2000) and pharmacological blockade of PI3K activity agents—enhances protein degradation pathways (Has- with the drug LY294002 blocks IGF-1-induced hypertroselgren, 1999; Jagoe and Goldberg, 2001; Mitch and phy in vitro (Rommel et al., 2001).”
• mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “…of mTOR signaling in the muscle revealed that mTORC1 activation is associated with muscle hypertrophy (Bodine et al., 2001) and that both IGF-1 and leucine promote hypertrophy through the activation of mTORC1 signaling in cultured cells and in mice (Anthony et al., 2000; Rommel et al., 2001).”
• mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “, 2001) and that both IGF-1and leucinepromote hypertrophy through the activation ofmTORC1 signaling in cultured cells and inmice (Anthony et al., 2000; Rommel et al., 2001).”
• IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1. (2004, methodology): “IGF-I and insulin are known to promote muscle hypertrophy via the PI3K-Akt pathway (44).”
• From mice to men: insights into the insulin resistance syndromes. (2006, background): “It phosphorylates glycogen synthase kinase 3 (GSK3), deactivating it (61).”