Figure 10

Depiction of potential AhR-dependent Akt activating pathways. In this study, we show that the presence of AhR reduced basal Akt phosphorylation. PI3K/Akt signaling pathway is activated by many types of cellular stimuli. Besides the canonical growth factor-mediated RTK/PI3K/Akt pathway, interactions between integrin and ECM can also transduce signals into the cell by activating the FAK/PI3K/Akt pathway; AhR may affect Akt phosphorylation through the regulation of these pathways. The red shaded area corresponds to the pathways not likely to be involved in AhR-dependent downregulation of Akt phosphorylation. The green shaded area represents the potential pathway by which AhR could modulate Akt phosphorylation. ECM extracellular matrix, GF growth factors, ITGA integrin subunit alpha, ITGB integrin subunit beta, FAK focal adhesion kinase, RTK receptor tyrosine kinase, PI3K phosphoinositide 3-kinase, AhR aryl hydrocarbon receptor, PIP₃ phosphatidylinositol 3,4,5-triphosphate, Akt AKT serine/threonine kinase, Pten phosphatase and tensin homolog, ROS reactive oxygen species.