Skip to main content
. Author manuscript; available in PMC: 2018 Apr 1.
Published in final edited form as: Trends Pharmacol Sci. 2017 Feb 14;38(4):339–362. doi: 10.1016/j.tips.2017.01.004

Figure 5. Targeting C. difficile oxin processing in host cells.

Figure 5

TcdA and TcdB are the two toxins produced by disease-associated C. difficile. Host processing of the toxins are mediated by endocytosis of the full-length toxin into an acidified compartment, leading to surface exposure of the cysteine protease domain (CPD) and glucosyltransferase domain (GTD). Interaction of the CPD with 1D-myo-inositol hexakisphosphate (IP6) leads to activation and autocatalysis of the linker region between the CPD and GTD. GTD is released into the host cytoplasm and alters intracellular signaling through glucosylation of Rho/Rac GTPase activity. Ebselen inhibits the protease activity of CPD, preventing the release of GTD into the host cytoplasm. The Ebselen inhibitor is in red. This model is derived and modified from Bender et al. [132]