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. 2006 Sep 11;74(12):6557–6570. doi: 10.1128/IAI.00591-06

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Copyright © 2006, American Society for Microbiology

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FIG. 2. — GAP activity of ExoS is not essential for apoptosis induction by PAK. HeLa cells were infected with the indicated PAK derivative strains (multiplicity of infection of 20) or left uninfected (CTRL). At 5 h postinfection, cells were collected, lysed, and subjected to caspase-3 assay. The exoS and exoT double mutant PAK (ST) was complemented with vector (ST/V) or with exoS (ST/S), exoS(E381A) [ST/s(EA)], exoS(R146K) [ST/s(RK)], or exoS(R146K/E381A) [ST/s(RKEA)] on the same vector. The data are means ± the SD of the ratios from four replicates. Significant differences between ST/V (V) and other PAK-derived strains are indicated (, P < 0.01; , P < 0.001).

Inline graphic — GAP activity of ExoS is not essential for apoptosis induction by PAK. HeLa cells were infected with the indicated PAK derivative strains (multiplicity of infection of 20) or left uninfected (CTRL). At 5 h postinfection, cells were collected, lysed, and subjected to caspase-3 assay. The exoS and exoT double mutant PAK (ST) was complemented with vector (ST/V) or with exoS (ST/S), exoS(E381A) [ST/s(EA)], exoS(R146K) [ST/s(RK)], or exoS(R146K/E381A) [ST/s(RKEA)] on the same vector. The data are means ± the SD of the ratios from four replicates. Significant differences between ST/V (V) and other PAK-derived strains are indicated (, P < 0.01; , P < 0.001).