The authors of “Endogenous RhoG is rapidly activated after epidermal growth factor stimulation through multiple guanine-nucleotide exchange factors” (Mol. Biol. Cell. [2010] 21, 1629–1642) would like to make a correction to their paper. In the legends to Figure 4 and Figure 6, the molar concentration units of some of the pharmacological inhibitors were misstated. Importantly, this correction does not change any of the conclusions or findings reported in the paper. The authors apologize for any inconvenience that the error may have caused. The corrected figure legends are shown below.
FIGURE 4: Effects of different kinase inhibitors on rapid activation of RhoG and Rac1 after EGF treatment. Serum-starved HeLa cells were stimulated with EGF for 30 s in the presence of different pharmacological inhibitors as indicated (pretreatment for 1 h). (A) MEK1/2 inhibitor, U0126 (10 μM). (B) PKCα inhibitor, Gö6976 (1.32 μM). (C) PI3K inhibitor, LY294002 (30 μM). (D) Src-family kinase inhibitor, SU6656 (2.5 μM). (E) EGFR kinase inhibitor, AG1478 (10 μM). RhoG.GTP and Rac1.GTP were measured by pull-down assays. The bar graphs summarize multiple independent experiments (n ≥ 3; error bars represent SEM). The asterisks indicate significant differences (p < 0.05).
FIGURE 6: Rapid phosphorylation of Vav2 and Vav3 after EGF stimulation. HeLa cells were stimulated with EGF (20 ng/ml) for the indicated times. Immunoprecipitated Vav2 and Vav3 were blotted for phosphotyrosine and Vav2 or Vav3, respectively. (A) Kinetics of Vav2 and Vav3 phosphorylation after different times of EGF stimulation. (B and C) Preceding EGF stimulation for 30 s, the cells were treated for 1 h with pharmacological inhibitors for different kinases: EGFR kinase inhibitor: AG1478 (10 μM); PI3K inhibitor, LY294002 (30 μM); MEK1/2 inhibitor, U0126 (10 μM); Src-family kinase inhibitor, SU6656 (2.5 μM).