Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 276, Issue 6, Pages 3840-3845Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M007819200
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Pasteurella multocida toxin (PRTT) is a highly potent mitogen for a variety of cell types. PMT has been shown to induce various cellular signaling processes, and it has been suggested to function through the heterotrimeric G-proteins G(q)/G(11). To analyze the role of G(q)/G(11) in the action of PMT, we have studied the effect of the toxin in G alpha (q)/G alpha (11) double-deficient fibroblasts as web as in fibroblasts lacking only G alpha (q) or G alpha (11). Interestingly, formation of inositol phosphates in response to PIT was exclusively dependent on Go, but not on the closely related G alpha (11). Although G alpha (q)/G alpha (11) double-deficient and G alpha (q)-deficient cells did not respond with any production of inositol phosphates to PMT, PMT was still able to induce various other cellular effects in these cells, including the activation of Rho, the Rho-dependent formation of actin stress fibers and focal adhesions, as well as the stimulation of c-Jun N-terminal kinase and extracellular signal-regulated kinase. These data show that PMT leads to a variety of cellular effects that are mediated only in part by the heterotrimeric G-protein G(q).
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