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Figure 3. Description of the phosphatidylinositol-3 kinase (PI3-K) pathway and the possible modulatory effect of triethylene glycol dimethacrylate (TEGDMA). Membrane receptors (ligand-dependent tyrosine kinase receptor, G-protein-coupled receptor) activate PI3-K to form the second-messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) by phosphorylating phosphatidylinositol-4,5-bisphosphate (PIP2). Then, PIP2 and PIP3 stimulate the phosphorylation (activation) of Akt (PKB/Akt). Akt is a key element in the control of substrates important for cell survival, cell cycle, protein synthesis, and metabolism. Activation of Akt by PI3-K is inhibited in the presence of TEGDMA. The possible links to elevated levels of reactive oxygen species (ROS) and a decrease in glutathione (GSH) levels remain to be elucidated. Tumor suppressor protein PTEN = phosphatase and tensin homologue; PH = pleckstrin homology; AFX, FKHR = forkhead transcription factors; BAD = pro-apoptotic factor of the Bcl-2 family; ASK-1 = apoptosis signal-regulating kinase 1; CREB = cAMP responsive element binding protein; IKK = inhibitor of NF-kappaB kinase; mTOR = mammalian target or rapamycin; GSK3 = glycogen synthase kinase 3; p21, p27 = cyclin-dependent kinase (cdk) inhibitors.
