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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Future Microbiol. 2010 Mar;5:431–453. doi: 10.2217/fmb.10.4

Figure 3. Shiga toxin-induced apoptotic signaling pathways in monocytic THP-1 cells.

Figure 3

Following toxin internalization, caspase 8 is rapidly activated, which in turn triggers caspase-dependent and mitochondrial-dependent apoptotic signaling cascades. Caspase 8 may directly activate caspase 3, which in turn may activate caspase 6 to create an amplication loop for activation of the executioner caspase. Caspase 8 also cleaves Bid. tBid molecules translocate to mitochondria and facilitate the release of cytochrome c. With dATP and Apaf-1, cytochrome c forms the apoptosome, leading to sequential activation of caspases 9 and 3. Apoptotic signaling requires the retrograde transport of holotoxin to the ER.

bid: BH3-domain-containing protein; ER: Endoplasmic reticulum; Gb3: Globotriaosylceramide; Stx: Shiga toxin.

Adapted with permission from [101]; © American Society for Microbiology.