A range of toxins can influence adenylyl cyclase activity either by direct interaction or through upstream signaling pathways. For instance, cholera toxin and pertussis toxin modulate G protein-coupled receptors (GPCRs) that, in turn, affect adenylyl cyclase. Cholera toxin, by ADP-ribosylating the Gs protein, leads to its persistent activation, resulting in continuous stimulation of adenylyl cyclase and excessive cAMP production. This elevation in cAMP levels can disrupt normal cellular processes, leading to conditions like severe diarrhea.
