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. 2012 Mar;32(5):981–991. doi: 10.1128/MCB.06410-11

Fig 1.

Fig 1

Chronic Ang II treatment induced AT1R/Cl4 cells to undergo EMT by a Src- and MEK-dependent signaling pathway. AT1R/Cl4 cells were cultured in 6-well plates and made quiescent by serum deprivation for 24 h and then maintained in DMEM/F12 medium containing 0.5% serum and Ang II (10−7 M) with or without the Src kinase inhibitor PP2 (5 μM) or the MEK inhibitor PD98059 (5 μM) for 4 days; during this period, such an EMT-inducing medium with or without inhibitors was prepared and changed daily for the cells. (A) Photographs were taken at ×100 magnification. (B) Cell lysates were subjected to immunoblotting with an antibody against E-cadherin or FSP1, followed by stripping and reprobing with an antibody to β-actin, respectively. (All of the data shown in these studies are representative of at least three separate experiments with similar results).