The mechanism of action of cholera toxin involves the ADP-ribosylation of the Gs protein, which is a regulatory protein that controls adenylate cyclase activity. Upon entering the intestinal epithelial cells, the A subunit of the toxin catalyzes the transfer of an ADP-ribose moiety to the Gs protein. This modification locks the Gs protein in its active form, leading to the continuous stimulation of adenylate cyclase. As a result, intracellular levels of cyclic AMP (cAMP) increase dramatically, causing the efflux of chloride ions and water into the intestinal lumen and resulting in diarrhea.
