La PI3 kinase, une activité critique pour la différenciation des cellules musculaires IGFs dépendante

Differential effects of Ras signaling through NFκB on skeletal myogenesis

“…The simplest interpretation of these data is that each of the Ras e ector pathways is su cient to block myogenesis. However, using constitutively active or dominant-negative signaling molecules and speci®c chemical inhibitors of Ras e ector pathways, we and others have shown that none of these Ras pathways, alone or in combination, duplicate the e ects of Ras in this system (Kaliman et al, 1996;Bennett and Tonks, 1997;Pinset et al, 1997;Weyman et al, 1997;Ramocki et al, 1998;Takano et al, 1998;Dorman and Johnson, 1999). For example, while constitutive activation of MAP kinase in the absence of Ras G12V e ectively blocks the early stages of muscle di erentiation (Bennett and Tonks, 1997;Ramocki et al, 1997;Dorman and Johnson, 1999), preventing MAP kinase activation in cells expressing Ras G12V or the T35S e ector domain variant does not reverse the nonmyogenic phenotype of the cells Weyman et al, 1997).…”

“…For example, while constitutive activation of MAP kinase in the absence of Ras G12V e ectively blocks the early stages of muscle di erentiation (Bennett and Tonks, 1997;Ramocki et al, 1997;Dorman and Johnson, 1999), preventing MAP kinase activation in cells expressing Ras G12V or the T35S e ector domain variant does not reverse the nonmyogenic phenotype of the cells Weyman et al, 1997). Similarly, whereas oncogenic Ras is known to activate PI3 kinase and the Rho GTPases in cells (Rodriguez-Viciana et al, 1994;Prendergast et al, 1995), exposure of myoblasts to chemical inhibitors of PI3 kinase blocks myogenesis (Kaliman et al, 1996;Pinset et al, 1997) and constitutive activation of RhoA enhances myogenesis Takano et al, 1998;Meriane et al, 2000). Therefore, the available experimental evidence has resulted in our embracing an alternative hypothesis ± that there is yet another pathway that mediates the e ects of Ras in this model system.…”

Requirement of BMP-2-induced Phosphatidylinositol 3-Kinase and Akt Serine/Threonine Kinase in Osteoblast Differentiation and Smad-dependent BMP-2 Gene Transcription

“…Recently a role of PI 3-kinase has been shown in TGF-␤-induced epithelial and endothelial cell survival and epithelial to mesenchymal transition (19,44,45) indicating that activation of serine/threonine kinase receptor utilizes this central lipid kinase as one of the signaling mechanisms similar to receptor tyrosine kinases. Recently PI 3-kinase has been implicated in myogenic differentiation (13,46,47). Also insulininduced adipocyte differentiation utilizes activation of PI 3-kinase pathway (48,49).…”

Phosphatidylinositol 3-Kinase Regulates Bone Morphogenetic Protein-2 (BMP-2)-induced Myocyte Enhancer Factor 2A-dependent Transcription of BMP-2 Gene in Cardiomyocyte Precursor Cells

“…3C). PI 3-kinase has been shown to regulate insulin-like growth factor-1-induced myogenic differentiation (34,36,40). Expression of constitutively active PI 3-kinase increased transcription of myogenin (40).…”