Skip to main content
. 2001 Oct 1;155(1):133–144. doi: 10.1083/jcb.200106148

Figure 5.

Figure 5.

ErbB2 activation induced by N. meningitidis leads to src activation and the phosphorylation of cortactin. (A and B) HBMECs (starved for 18 h) were either uninfected (−) or infected with the wild-type (WT), the PilT-defective mutant (PilT), or the PilE-defective mutant (PilE) of the 2C43 strain of N. meningitidis for 4 h before lysis. (C–E) HBMECs starved for 18 h were pretreated for 2 h with either 5 μM PP2 or 5 μM AG1478 (+) or left untreated (−). Cells were either noninfected (NT) or infected with the wild-type 2C43 or the ROU strains as indicated for 4 h before lysis. PP2 and AG1478 treatments were maintained during infection. As control, cells pretreated the same way were stimulated with 10 ng/ml EGF for 3 min before lysis. (A, D, and E) Cortactin was immunoprecipitated and immunoblotted with an antiphosphotyrosine antibody (4G10) (top). Blots were reprobed with an anticortactin antibody (bottom) to show that similar protein levels were immunoprecipitated. (B and C) Src was immunoprecipitated and subjected to either an autophosphorylation assay (B) or an in vitro kinase assay using acid-denaturated enolase as a substrate (C). Three independent experiments were carried out with similar results and representative results from one experiment are shown.