Fig. 5.

T3 regulates Src/FAK/PI3K complex formation. T-47D breast cancer cells were exposed for 20 min to T3 (1 nM) in the presence or absence of the Src inhibitor (PP2 10 μM), the PI3K inhibitor wortmannin (WM 30 nM), FAK inhibitor (FAKi 1 μM), or the MAPK inhibitor PD98059 (PD 5 mM). a, b Tyr397- FAK phosphorylation was evaluated through Western blot analysis. c Breast cancer cells treated with T3 for 20 min in the presence or absence of FAK inhibitor and the inhibitor of the extracellular regulated kinase 1/2 (ERK1/2), PD98059. Cell contents of total or phosphorylated ERK1/2 are shown. d, e T-47D breast cancer cells were exposed to T3 (1 nM) for 20 min in the presence or absence of PP2, WM, and FAKi. Cell protein extracts were immunoprecipitated with an antibody vs. FAK (d) and p85alpha (e). IPs were assayed for co-immunoprecipitation with Src, FAK, and p85α. Membranes were re-blotted for the immunoprecipitated protein to show equal input. The experiments were performed in triplicate; representative images are shown. CON control