Special Issue "Heat-Stable Enterotoxins"
Deadline for manuscript submissions: closed (15 November 2017)
Diarrheagenic bacterial heat-stable enteroxins (STs) are a major cause of morbidity and mortality worldwide. This family of homologous toxins induces diarrhea by recapitulating the structure of the endogenous intestinal paracrine hormones guanylin and uroguanylin. This molecular mimicry confers on STs the ability to co-opt signaling through the intestinal receptor guanylate cyclase C (GCC), which regulates epithelial fluid and electrolyte balance. Beyond secretion, GCC and its cognate ligands have emerged as important regulators of fundamental homeostatic processes which organize the intestinal crypt-surface axis. Moroever, dysregulation of this signaling system plays a key role in pathophysiological processes beyond infectious diarrhea, including intestinal transformation, mucosal inflammation, and gut–brain satiety signaling. Understanding the normal function of the GCC signaling axis, and mechanisms underlying its pathophysiological disruption, provides unique opportunities to create therapeutic solutions using toxins and their cognate receptors for major diseases including infectious diarrhea, chronic constipation, colorectal cancer, inflammatory bowel disease and obesity.
Prof. Dr. Scott A. Waldman
Manuscript Submission Information
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- heat-stable enterotoxins;
- guanylate cyclase C;
- secretory diarrhea;
- chronic constipation;
- colorectal cancer;
- irritable bowel syndrome (constipation type);
- inflammatory bowel disease;