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• W1495826882 endingPage "733" @default.
• W1495826882 startingPage "729" @default.
• W1495826882 abstract "Pathogenic Escherichia coli are responsible for a variety of diseases, including diarrhoea, haemolytic uraemic syndrome, kidney infection, septicaemia, pneumonia and meningitis. Toxins called cytotoxic necrotizing factors (CNFs) are among the virulence factors produced by uropathogenic (CNF1) or enteropathogenic (CNF2) E. coli strains that cause diseases in humans and animals, respectively. CNFs induce an increase in the content of actin stress fibres and focal contacts in cultured cells. Effects of CNFs on the actin cytoskeleton correlated with a decrease in the electrophoretic mobility of the GTP-binding protein Rho and indirect evidence indicates that CNF1 might constitutively activate Rho. Here we show that CNF1 catalyses the deamidation of a glutamine residue at position 63 of Rho, turning it into glutamic acid, which inhibits both intrinsic GTP hydrolysis and that stimulated by its GTPase-activating protein (GAP). Thus, this deamidation of glutamine 63 by CNF1 leads to the constitutive activation of Rho, and induces the reorganization of actin stress fibres. To our knowledge, CNF1 is the first example of a bacterial toxin acting by deamidation of a specific target protein." @default.
• W1495826882 created "2016-06-24" @default.
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• W1495826882 date "1997-06-01" @default.
• W1495826882 modified "2023-10-14" @default.
• W1495826882 title "Toxin-induced activation of the G protein p21 Rho by deamidation of glutamine" @default.
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• W1495826882 doi "https://doi.org/10.1038/42743" @default.
• W1495826882 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9192901" @default.
• W1495826882 hasPublicationYear "1997" @default.
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