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Figure 1B shows a decrease in cell Fluorescence when treated with a virulent strain of shiga toxin.

Figure 6 shows a scheme of the NAD+ dependent ADP-ribosylation of CTA1 in the cytosol.

Figure 3.

Figure 2A.

Figure 1B and Table 1.

Figure 8 shows the Oxydoreductase activity of PDI using ricin.

Figure 1C and table 1.

Figure 1D and Table 1.

Figure 7 shows a dose response increase in cAMP level in presence of cholera toxin (CT).

Figure 2 shows a decrease level of protein synthesis in presence of shiga toxin 2 (Stx2).

Figure 6.

Figure 3.

Figure 1.

Figure 3.

Figure 8A.

Figure 4.

Figure 1 shows a decrease of cell viability with increasing concentration of Ricin.

Figure 6 (lane 2 and 3). CTA get reduced in the presence of PDI (lane 3). Lane 2 is without PDI.

Figure 6.

Figure 6.

Figure 8A.

Figure 8A.

Figure 4.

Figure 4.

Figure 6 (lane 2 and 3). CTA get reduced in the presence of PDI (lane 3). Lane 2 is without PDI.

Figure 1B and Table 1.

Figure 1C and table 1.

Figure 1C and table 1.

Figure 1D and Table 1.

Figure 1D and Table 1.

Figure 3.

Figure 1.

Figure 2.

Figure 3.

Table 1.

Table 1.

Figure 1.

Ricin toxin binds to the ribosome thereby blocks protein synthesis and cause cell death (Apoptosis). Figure 1 shows a drastic decrease in cell viability with increasing concentration of Ricin.

In order for Ricin to intoxicate the host cell, its disulfide bridge has to be reduced. It has been shown that protein disulfide isomerase (PDI) has the ability to reduce the disulfide bond. However, reduction can still occur even when PDI is depleted, suggesting that other proteins are also responsible to reduce Ricin. Transmenbrane Thioredoxin related protein (TMX) has been found to reduce Ricin. Figure 2 shows that TMX is needed to reduce Ricin. In Lane 1 when TMX is added, Ricin is reduced (the RTA band), whereas in lane 3 with no TMX, Ricin is not reduced.