The identification of the Ras superfamily of small molecular weight GTPases (G-proteins) has opened up new fields in cancer biology, immunity and infectious disease research. Because of their ubiquitous role in cellular homeostasis, small G-proteins are common targets for several pathogens, including bacteria. It is well known that pathogenic bacteria have evolved virulence factors that chemically modify GTPases or directly mimic the activities of key regulatory proteins. However, recent studies now suggest that bacterial 'effector' proteins can also mimic the activities of Ras small G-proteins despite their lack of guanine nucleotide binding or GTPase enzymatic activity. The study of these unique pathogenic strategies continues to reveal novel mechanistic insights into host cellular communication networks and the role of small G-protein signalling during human infectious disease.
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