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. 2010 May 7;285(28):21625–21635. doi: 10.1074/jbc.M110.103010

FIGURE 2.

FIGURE 2.

RAS and ERK activation are uncoupled in Chlamydia-infected cells. A, HEK-Tth cells were treated 30 min postinfection with the farnesyl transferase inhibitor (FTI) l-744/832 or the MEK inhibitor U0126. At 24 h, cells were harvested, and the levels of active ERK were assessed by immunoblots. Note increase in active ERK levels in response to infection despite FTI treatment. Control experiments show FTI-mediated inhibition of ERK phosphorylation in response to serum growth factors. B, HeLa cells were transfected with EGFP empty vector (DNA expression control), RAS, or dominant-negative RAS17N expression constructs for 20 h prior to infection with L2 or treatment with EGF. Transfection of RAS17N did not prevent the accumulation of active ERK in response to Chlamydia infection. C, infected HeLa cells were treated with U0126 and levels of RAS-GTP were assessed as in Fig. 1A. Inhibition of ERK activation did not prevent the accumulation of RAS-GTP in response to infection. All blots are representative from at least three independent experiments.