Cholera 12 The American Journal of Medicine

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Cholera 12 The American Journal of Medicine Jean-Pierre Raufman The American Journal of Medicine Volume 104, Issue 4, Pages 386-394 (April 1998) DOI: 10.1016/S0002-9343(98)00076-X

Fig. 1 Cholera toxin (CT) and zona occludens toxin (ZOT) are released from Vibrio cholera. CT binds to GM1 ganglioside receptors on the apical surface. The cholera toxin molecule contains A1 and A2 subunits, and five B subunits that bind to the oligosaccharide portion of GM1. GM1 is anchored in the apical plasma membrane by its ceramide moiety. Cholera toxin subunits bound to GM1 receptors enter the cell within endosomes. The acidic endosomes move retrograde along the secretory pathway to the transGolgi network and the endoplasmic reticulum (ER) and then antegrade to the adenylyl cyclase-G protein complex located on the basolateral membrane. The A1 subunit of cholera toxin catalyzes ribosylation of the α subunit of a guanine nucleotide stimulatory protein (Gs). N, nucleus. The American Journal of Medicine 1998 104, 386-394DOI: (10.1016/S0002-9343(98)00076-X)

Fig. 2 Cholera toxin-induced ribosylation of Gsα results in activation of adenylyl cyclase and a 100-fold increase in cyclic adenosine monophosphate (cAMP) production. cAMP activates protein kinase A, which then phosphorylates and activates the apical choloride channel. The American Journal of Medicine 1998 104, 386-394DOI: (10.1016/S0002-9343(98)00076-X)

Fig. 3 Current models of cystic fibrosis transmembrane regulator (CFTR) indicate two nucleotide-binding domains (NBD) and one regulatory domain (R). Increases in cyclic adenosine monophosphate (cAMP) result in PKA-mediated phosphorylation of the regulatory domain, thereby opening the channel. Binding of adenosine triphosphate (ATP) to at least one nucleotide-binding domain is necessary for activation of the channel. As indicated, basolateral membrane ion transport is mediated by a K+ channel, a Na+ pump, and a Na+−K+−2Cl− cotransporter. Potential difference is shown for the luminal, cellular, and interstitial compartments. The American Journal of Medicine 1998 104, 386-394DOI: (10.1016/S0002-9343(98)00076-X)

The American Journal of Medicine 1998 104, 386-394DOI: (10 The American Journal of Medicine 1998 104, 386-394DOI: (10.1016/S0002-9343(98)00076-X)