Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0740441 (acute diarrhea)
 2,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heat stable enterotoxins (STs) are low molecular-weight peptides secreted by enterotoxigenic bacteria. One type of these enterotoxins (STa) induces intestinal secretion leading to acute diarrhea by binding to a membrane form of guanylate cyclase. We have isolated a cDNA from a human colonic cell line, T84, encoding for a guanylate cyclase-coupled enterotoxin receptor (STaR). The predicted amino acid sequence of the human STa receptor is 81% identical with the previously cloned enterotoxin receptor (GC-C) from rat intestine. COS-7 cells transiently transfected with the cloned cDNA expressed specific concentration-dependent response to STa as measured by cyclic GMP accumulation and is about 20 times more sensitive to the stimulation by STa than has been shown for GC-C.
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PMID:Isolation and expression of a guanylate cyclase-coupled heat stable enterotoxin receptor cDNA from a human colonic cell line. 171 70

Diarrheal diseases caused by microorganisms and their toxins are a major cause of mortality and morbidity throughout the world. Acute diarrhea is mainly caused due to increased intestinal secretion, commonly as a result of infection with enterotoxin producing organisms (enterotoxigenic Escherichia coli, Vibrio cholera) or due to decreased intestinal absorption from infection with organisms that damage the intestinal epithelium (enteropathogenic E. coli sp., Shigella sp., Salmonella sp.) The studies of the impact of enteric pathogens and their virulence factors exert their effect by producing toxins, called bacterial toxins. The protein toxins are produced by diverse group of bacteria. Most of the bacterial toxins exert their effect through involvement of ADP-ribosylation proteins; otherwise essential for several cellular functions while other toxins involve guanylate cyclase systems or calcium and protein kinases for their ultimate action.
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PMID:Modulation of gut physiology through enteric toxins. 1461 51