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Gene Review

Cdc42  -  cell division cycle 42

Rattus norvegicus

Synonyms: Cell division control protein 42 homolog
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Disease relevance of Cdc42


High impact information on Cdc42


Chemical compound and disease context of Cdc42

  • Although Rac/Cdc42 GTPase inhibition led to F-actin disruption, direct cytoskeletal disassembly with Clostridium botulinum C2 toxin was insufficient to induce c-Jun phosphorylation or apoptosis [5].
  • Infection of hepatocytes with poly-L-lysine-coated adenoviruses coupled to constructs to express either dominant negatives Ras N17, Rac1 (N17), Cdc42 (N17), SEK1-, or JNK1- blunted the abilities of glucose, TNFalpha, or HGF to increase JNK1 activity, to increase phosphorylation of c-Jun at serine 63, and to stimulate DNA synthesis [9].
  • Exposure of normal rat islets or isolated beta (HIT-T15) cells to Clostridium difficile toxins A and B catalyzed the glucosylation (and thereby the inactivation) of Rac, Cdc42, and Rho endogenous to beta cells; concomitantly, either toxin reduced glucose- or potassium-induced insulin secretion from rat islets and HIT cells [10].
  • Indeed, inhibition of the small GTPases RhoA, Rac, and Cdc42 (by Clostridium difficile toxin B) prevents the hypotonicity-induced reorganization of the actin cytoskeleton, whereas inhibition of RhoA alone (by C. limosum C3 exoenzyme) does not preclude this rearrangement [11].
  • In contrast, the cytotoxic Clostridium difficile toxin B (ToxB), which glucosylated the Rho-subtype family members RhoA and Cdc42, blocked or reduced antigen- or calcium ionophore-mediated [3H]serotonin release, respectively, and decreased tyrosine phosphorylation of a 110 kDa protein [12].

Biological context of Cdc42


Anatomical context of Cdc42

  • Rin mutant proteins, in which the mutation disrupted association with CaM, failed to induce neurite outgrowth irrespective of Rac/Cdc42 activation [15].
  • This inhibition was mediated by reorganization of the actin cytoskeleton by Rac and Cdc42 through IQGAP1, an actin filament-binding protein and a downstream target of Rac and Cdc42 [13].
  • Small GTPase Rin induces neurite outgrowth through Rac/Cdc42 and calmodulin in PC12 cells [15].
  • By contrast, dynein-independent transport to the Golgi complex is insensitive to mutant Cdc42 [16].
  • Targeting of the myosin-I myr 3 to intercellular adherens type junctions induced by dominant active Cdc42 in HeLa cells [17].

Associations of Cdc42 with chemical compounds


Physical interactions of Cdc42


Regulatory relationships of Cdc42


Other interactions of Cdc42

  • FRET imaging also delineated a difference between the localization of activated Rac1 and that of Cdc42 within the neurite tips [14].
  • These results indicate the important role of the Rac/Cdc42-IQGAP1 system in the dynamic organization and maintenance of the E-cadherin-based AJs [13].
  • Thus, N-WASP is thought to be a general regulator of the actin cytoskeleton indispensable for neurite extension, which is probably caused through Cdc42 signaling and Arp2/3 complex-induced actin polymerization [23].
  • Binding of Cdc42 to phospholipase D1 is important in neurite outgrowth of neural stem cells [20].
  • Previous studies had shown that toxin B, an inhibitor of Rho, Rac and Cdc42, suppressed Cox-2 induction [1].

Analytical, diagnostic and therapeutic context of Cdc42


  1. Role of Rac and Cdc42 in lysophosphatidic acid-mediated cyclo-oxygenase-2 gene expression. Hahn, A., Barth, H., Kress, M., Mertens, P.R., Goppelt-Struebe, M. Biochem. J. (2002) [Pubmed]
  2. Dystrophin-glycoprotein complex and Ras and Rho GTPase signaling are altered in muscle atrophy. Chockalingam, P.S., Cholera, R., Oak, S.A., Zheng, Y., Jarrett, H.W., Thomason, D.B. Am. J. Physiol., Cell Physiol. (2002) [Pubmed]
  3. PAR-6-PAR-3 mediates Cdc42-induced Rac activation through the Rac GEFs STEF/Tiam1. Nishimura, T., Yamaguchi, T., Kato, K., Yoshizawa, M., Nabeshima, Y., Ohno, S., Hoshino, M., Kaibuchi, K. Nat. Cell Biol. (2005) [Pubmed]
  4. Mechanism of N-WASP activation by CDC42 and phosphatidylinositol 4, 5-bisphosphate. Rohatgi, R., Ho, H.Y., Kirschner, M.W. J. Cell Biol. (2000) [Pubmed]
  5. An essential role for Rac/Cdc42 GTPases in cerebellar granule neuron survival. Linseman, D.A., Laessig, T., Meintzer, M.K., McClure, M., Barth, H., Aktories, K., Heidenreich, K.A. J. Biol. Chem. (2001) [Pubmed]
  6. Integrin-mediated activation of Cdc42 controls cell polarity in migrating astrocytes through PKCzeta. Etienne-Manneville, S., Hall, A. Cell (2001) [Pubmed]
  7. The interaction between N-WASP and the Arp2/3 complex links Cdc42-dependent signals to actin assembly. Rohatgi, R., Ma, L., Miki, H., Lopez, M., Kirchhausen, T., Takenawa, T., Kirschner, M.W. Cell (1999) [Pubmed]
  8. Cdc42 regulates GSK-3beta and adenomatous polyposis coli to control cell polarity. Etienne-Manneville, S., Hall, A. Nature (2003) [Pubmed]
  9. The Ras/Rac1/Cdc42/SEK/JNK/c-Jun cascade is a key pathway by which agonists stimulate DNA synthesis in primary cultures of rat hepatocytes. Auer, K.L., Contessa, J., Brenz-Verca, S., Pirola, L., Rusconi, S., Cooper, G., Abo, A., Wymann, M.P., Davis, R.J., Birrer, M., Dent, P. Mol. Biol. Cell (1998) [Pubmed]
  10. Evidence for differential roles of the Rho subfamily of GTP-binding proteins in glucose- and calcium-induced insulin secretion from pancreatic beta cells. Kowluru, A., Li, G., Rabaglia, M.E., Segu, V.B., Hofmann, F., Aktories, K., Metz, S.A. Biochem. Pharmacol. (1997) [Pubmed]
  11. Hypotonicity induces membrane protrusions and actin remodeling via activation of small GTPases Rac and Cdc42 in Rat-1 fibroblasts. Carton, I., Hermans, D., Eggermont, J. Am. J. Physiol., Cell Physiol. (2003) [Pubmed]
  12. ADP-ribosylating and glucosylating toxins as tools to study secretion in RBL cells. Prepens, U., Just, I., Hofmann, F., Aktories, K. Adv. Exp. Med. Biol. (1997) [Pubmed]
  13. Endocytosis of E-cadherin regulated by Rac and Cdc42 small G proteins through IQGAP1 and actin filaments. Izumi, G., Sakisaka, T., Baba, T., Tanaka, S., Morimoto, K., Takai, Y. J. Cell Biol. (2004) [Pubmed]
  14. Spatio-temporal regulation of Rac1 and Cdc42 activity during nerve growth factor-induced neurite outgrowth in PC12 cells. Aoki, K., Nakamura, T., Matsuda, M. J. Biol. Chem. (2004) [Pubmed]
  15. Small GTPase Rin induces neurite outgrowth through Rac/Cdc42 and calmodulin in PC12 cells. Hoshino, M., Nakamura, S. J. Cell Biol. (2003) [Pubmed]
  16. Coatomer-bound Cdc42 regulates dynein recruitment to COPI vesicles. Chen, J.L., Fucini, R.V., Lacomis, L., Erdjument-Bromage, H., Tempst, P., Stamnes, M. J. Cell Biol. (2005) [Pubmed]
  17. Targeting of the myosin-I myr 3 to intercellular adherens type junctions induced by dominant active Cdc42 in HeLa cells. Stöffler, H.E., Honnert, U., Bauer, C.A., Höfer, D., Schwarz, H., Müller, R.T., Drenckhahn, D., Bähler, M. J. Cell. Sci. (1998) [Pubmed]
  18. Serotonin-induced regulation of the actin network for learning-related synaptic growth requires Cdc42, N-WASP, and PAK in Aplysia sensory neurons. Udo, H., Jin, I., Kim, J.H., Li, H.L., Youn, T., Hawkins, R.D., Kandel, E.R., Bailey, C.H. Neuron (2005) [Pubmed]
  19. PAK promotes morphological changes by acting upstream of Rac. Obermeier, A., Ahmed, S., Manser, E., Yen, S.C., Hall, C., Lim, L. EMBO J. (1998) [Pubmed]
  20. Binding of Cdc42 to phospholipase D1 is important in neurite outgrowth of neural stem cells. Yoon, M.S., Cho, C.H., Lee, K.S., Han, J.S. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  21. Delineation of the Cdc42/Rac-binding domain of p21-activated kinase. Thompson, G., Owen, D., Chalk, P.A., Lowe, P.N. Biochemistry (1998) [Pubmed]
  22. Conformational switch and role of phosphorylation in PAK activation. Buchwald, G., Hostinova, E., Rudolph, M.G., Kraemer, A., Sickmann, A., Meyer, H.E., Scheffzek, K., Wittinghofer, A. Mol. Cell. Biol. (2001) [Pubmed]
  23. Essential role of neural Wiskott-Aldrich syndrome protein in neurite extension in PC12 cells and rat hippocampal primary culture cells. Banzai, Y., Miki, H., Yamaguchi, H., Takenawa, T. J. Biol. Chem. (2000) [Pubmed]
  24. PACAP activates Rac1 and synergizes with NGF to activate ERK1/2, thereby inducing neurite outgrowth in PC12 cells. Sakai, Y., Hashimoto, H., Shintani, N., Katoh, H., Negishi, M., Kawaguchi, C., Kasai, A., Baba, A. Brain Res. Mol. Brain Res. (2004) [Pubmed]
  25. Integrin-mediated signals regulated by members of the rho family of GTPases. Clark, E.A., King, W.G., Brugge, J.S., Symons, M., Hynes, R.O. J. Cell Biol. (1998) [Pubmed]
  26. Molecular cloning of a new member of the p21-Cdc42/Rac-activated kinase (PAK) family. Manser, E., Chong, C., Zhao, Z.S., Leung, T., Michael, G., Hall, C., Lim, L. J. Biol. Chem. (1995) [Pubmed]
  27. Fibroblast transformation by Fps/Fes tyrosine kinases requires Ras, Rac, and Cdc42 and induces extracellular signal-regulated and c-Jun N-terminal kinase activation. Li, J., Smithgall, T.E. J. Biol. Chem. (1998) [Pubmed]
  28. Molecular cloning and sequencing of rat Cdc42 GTPase cDNA. Han, J.S., Kim, J.H., Kim, J.G., Park, J.B., Noh, D.Y., Lee, K.H. Exp. Mol. Med. (2000) [Pubmed]
  29. Modulation of Rho and cytoskeletal protein attachment to membranes by a prenylcysteine analog. Desrosiers, R.R., Gauthier, F., Lanthier, J., Béliveau, R. J. Biol. Chem. (2000) [Pubmed]
  30. Inhibition of Fc epsilon-RI-mediated activation of rat basophilic leukemia cells by Clostridium difficile toxin B (monoglucosyltransferase). Prepens, U., Just, I., von Eichel-Streiber, C., Aktories, K. J. Biol. Chem. (1996) [Pubmed]
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