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By Alistair J. Lax

Bacterial pollution that act within cells have interaction very in particular with key parts of the mobile and a few even control the phone in sophisticated methods for his or her personal reasons. those effective pollutants, defined during this 2005 publication, may be of curiosity to either microbiologists and cellphone biologists. a few of these pollutants are traditional multidomain pollutants which are self-programmed to go into cells. Others are added by way of style III mechanisms, frequently as a package deal of effective molecules. The molecular pursuits for a majority of these pollutants mediate sign transduction and the telephone cycle to manage the the most important techniques of telephone progress, telephone department and differentiation. hence those effective pollution should not simply liable for disorder, but additionally supply a strong set of instruments with which to interrogate the biology of the cellphone. moreover such pollution may well act on to advertise carcinogenesis and consequently their examine can also be of curiosity in a much wider context.

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Extra info for Bacterial Protein Toxins: Role in the Interference with Cell Growth Regulation (Advances in Molecular and Cellular Microbiology)

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Direct stimulation of the guanine nucleotide exchange activity of p115 RhoGEF by Gα 13 . Science, 280, 2112–2114. Higgins T E, Murphy A C, Staddon J M, Lax A J, and Rozengurt E (1992). Pasteurella multocida toxin is a potent inducer of anchorage-independent cell growth. Proc. Natl. Acad. Sci. USA, 89, 4240–4244. Hoskins I C, Thomas L H, and Lax A J (1997). Nasal infection with Pasteurella multocida causes proliferation of bladder epithelium in gnotobiotic pigs. Vet. , 140, 22. James S R and Downes C P (1997).

PMT pre-treatment failed to produce an additive response, suggesting that a common G-protein pool mediated both effects. In contrast, PMT pre-treatment produced an additive Erk1/2 phosphorylation with the Gi -coupled LPA receptor, indicating 19 the pasteurella multocida toxin that Gi was not involved in the PMT response. Interestingly, the PMT effect was not additive with the EGF receptor. These results were confirmed using specific inhibitors of G-protein function. Erk activation by PMT was unaffected by the Gi inhibitor, pertussis toxin, but was significantly attenuated by the expression of Gq/11 inhibitory peptides (the C-terminal fragment of Gα q , Gα q -(305–359), and an inactive mutant of the G-protein-coupled receptor kinase GRK2, GRK2(K2220R)).

180, 15–20. Sprang S R (1997). G protein mechanisms: Insights from structural analysis. Annu. Rev. , 66, 639–678. Staddon J M, Barker C J, Murphy A C, Chanter N, Lax A J, Michell R H, and Rozengurt E (1991a). Pasteurella multocida toxin, a potent mitogen, increases inositol 1,4,5-trisphosphate and mobilizes Ca2+ in Swiss 3T3 cells. J. Biol. , 266, 4840–4847. Staddon J M, Bouzyk M M, and Rozengurt E (1991b). A novel approach to detect toxin-catalyzed ADP-ribosylation in intact cells: Its use to study the action of Pasteurella multocida toxin.

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