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. 2011 Dec 12;195(6):931–942. doi: 10.1083/jcb.201108081

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© 2011 Ashida et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 3. — Bacterial manipulation of host pro-survival pathway. M. tuberculosis activates host anti-apoptotic signaling by up-regulating the anti-apoptosis genes Mcl-1, bfl1, and FLIP. NuoG dampens Nox2-mediated host signaling, resulting in the inhibition of apoptosis. Legionella deliver LegK1 and LnaB, which enhance the pro-survival activity of NF-κB. Shigella invasion of the epithelium results in mitochondria permeability transition (MPT)−dependent ROS production and necrosis-like cell death, which is counterbalanced by the NOD1−RIP2−NF-κB−Bcl2 pro-survival pathway. PGN, peptidoglycan. Salmonella deliver SopB and AvrA via the T3SS, and they inhibit apoptosis by activating the PI3K–Akt pro-survival pathway via inositol phosphate activity and by preventing JNK pro-cell death signaling via acetyltransferase activity, respectively. EPEC also targets JNK signaling by delivering NleD, which uses its metalloprotease activity to cleave JNK, thereby inhibiting cell death.