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 Woodgett Lab 

 

Rac and Cdc42

 
 

Rac and Cdc42 are Rho-like GTPases and bind proteins such as the PAK kinases and the Wiscott-Aldrich Syndrome protein (WASP). Introduction of GTP clamped (active) forms of these proteins into cells causes activation of both the SAPK and p38 pathways via an as yet unknown mechanism. Transforming G proteins also induce SAPK

References

  • Symons, M. (1996) Rho family GTPases: the cytoskeleton and beyond. TIBS, 21.
  • Bagrodia S, Derijard B, Davis RJ and Cerione RA (1995) Cdc42 and PAK mediated signaling leads to Jun kinase and p38 mitogen-activated protein kinase activation. J. Biol. Chem. 270, 27995-27998
  • Coso, O.A., Chiariello, M., Yu, J.-C., Teramoto, H., Crespo, P., Xu, N., Miki, T. & Gutkind, S. (1995) The small GTP-binding proteins Rac1 and Cdc42 regulate the activity of the JNK/SAPK signaling pathway. Cell 81, 1137-1146
  • Minden, A., Lin, A., Claret, F.X., Abo, A. and Karin, M. (1995) Selective activation of the JNK signaling cascade and c-Jun transcriptional activity by the small GTPases Rac and Cdc42Hs. Cell 81,1147-1157.
  • Coso, O.A., Teramoto, H., Simonds, W.F. and Gutkind, J.S. (1996) Signaling from G protein-coupled receptors to c-Jun kinase involves beta gamma subunits of heterotrimeric G proteins acting on a Ras and Rac1-dependent pathway. J. Biol. Chem. 271, 3963-3966.
  • Coso, O.A., Chiariello, M., Kalinec, G., Kyriakis, J.M., Woodgett, J. and Gutkind, J.S. (1995) Transforming G protein-coupled receptors potently activate JNK (SAPK). Evidence for a divergence from the tyrosine kinase signaling pathway. J. Biol. Chem. 270, 5620-5624.
  • Symons, M., Derry, J.M., Karlak, B., Jiang, S., Lemahieu, V., Mccormick, F., Francke, U. and Abo, A. (1996) Wiskott-Aldrich syndrome protein, a novel effector for the GTPase CDC42Hs, is implicated in actin polymerization. Cell84,723-734.
 

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