Short Article The IGF-1/PI3K/Akt Pathway Prevents Expression of Muscle Atrophy-Induced Ubiquitin Ligases by Inhibiting FOXO Transcription Factors

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Summary membrane phospholipid phosphatidylinositol-4,5-bis- phosphate to phosphatidylinositol-3,4,5-trisphosphate, Skeletalmusclesizedependsuponadynamicbalance creating a lipid binding site on the cell membrane forbetween anabolic (or hypertrophic) and catabolic (or a serine/threonine kinase called Akt (or PKB—protein atrophic) processes. Previously, no link between the kinase B). The subsequent translocation of Akt to themolecular mediators of atrophy and hypertrophy had membrane facilitates its phosphorylation and activation been reported. We demonstrate a hierarchy between by the kinase PDK-1 (Cantley, 2002; Datta et al., 1999;the signals which mediate hypertrophy and those Vivanco and Sawyers, 2002). Cell growth and survival which mediate atrophy: the IGF-1/PI3K/Akt pathway, inavarietyoftissuesandcelltypesinresponsetoIGF-1,which has been shown to induce hypertrophy, pre- insulin, and other growth factors is critically mediated ventsinductionofrequisiteatrophymediators,namely by Akt (Datta et al., 1999; Vivanco and Sawyers, 2002).the muscle-specific ubiquitin ligases MAFbx and

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