Cholera toxin ADP-ribosylates G proteins, causing massive fluid secretion from the lining of the small intestine, resulting in life-threatening diarrhea.
P. aeruginosa ADP-ribosylates cytoskeleton and GTP-binding proteins.
Diphtheria toxin - It catalyzes the ADP-ribosylation of eukaryotic elongation factor-2 (eEF2), inactivating this protein.
Pertussis toxin - PT catalyzes the ADP-ribosylation of the α subunits of the heterotrimeric G proteins Gi, Go, and Gt. This prevents the G proteins from interacting with G protein-coupled receptors on the cell membrane, thus interfering with intracellular communication. The Gi subunits remain locked in their GDP-bound, inactive state, thus unable to inhibit adenyl cyclase activity, leading to increased cellular concentrations of cAMP.
Increased intracellular cAMP affects normal biological signaling. The toxin causes several systemic effects, among which is an increased release of insulin, causing hypoglycemia. Whether the effects of pertussis toxin are responsible for the paroxysmal cough remains unknown.