The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

RAC1  -  ras-related C3 botulinum toxin substrate 1...

Canis lupus familiaris

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of RAC1

  • Cdc42 and Rac1 regulate late events in Salmonella typhimurium-induced interleukin-8 secretion from polarized epithelial cells [1].
  • Cell vacuolation induced by the VacA cytotoxin of Helicobacter pylori is regulated by the Rac1 GTPase [2].
  • Tachycardia also augmented the association of rac1 and the NADPH oxidase cytosolic subunit p47(phox) to the microsomal fraction, without modifying the content of the membrane integral subunit gp91(phox) [3].

High impact information on RAC1

  • Finally, we show that ARF6-mediated recruitment of Nm-23-H1 to cell junctions is accompanied by a decrease in the cellular levels of Rac1-GTP, consistent with previous findings that Nm23-H1 down-regulates activation of Rac1 [4].
  • Here, we report that orientation of apical polarity in developing Madin-Darby canine kidney (MDCK) epithelial cysts requires the small GTPase Rac1 and the basement membrane component laminin [5].
  • We suggest that Rac1 and RhoA are involved in the transition of epithelial cells from a fibroblastic to a polarized structure and function by direct and indirect regulation of actin and actin-associated membrane protein organizations [6].
  • Structural and functional regulation of tight junctions by RhoA and Rac1 small GTPases [7].
  • Effects of regulated expression of mutant RhoA and Rac1 small GTPases on the development of epithelial (MDCK) cell polarity [6].

Biological context of RAC1

  • Both constitutively active and dominant negative RhoA or Rac1 perturbed TJ gate function (transepithelial electrical resistance, tracer diffusion) in a dose-dependent and reversible manner [7].
  • We also investigated the signaling pathways that are activated by Rac1 to stimulate cell survival [8].
  • This is followed by a steady increase in Rac1 and ARF6 activation and cell migration [9].
  • Here we show that constitutive activation of Rac1 inhibits anoikis in Madin-Darby canine kidney (MDCK) epithelial cells [8].
  • These results show that in polarized MDCK cells activated Rac1 may regulate the rate of endocytosis from both membrane domains and that expression of dominant active Rac1V12 specifically alters postendocytic and biosynthetic membrane traffic directed to the apical, but not the basolateral, membrane [10].

Anatomical context of RAC1

  • Ezrin regulates E-cadherin-dependent adherens junction assembly through Rac1 activation [11].
  • Together with Rac1 activation, we observed an accumulation of E-cadherin in intracellular compartments and a concomitant decrease in the level of E-cadherin present at the plasma membrane [11].
  • Rac1 is a member of the Rho family of small GTP-binding proteins that regulate reorganization of the actin cytoskeleton and intracellular signal transduction and are being shown increasingly to play a role in membrane trafficking events [2].
  • Madin-Darby canine kidney (MDCK) cells expressing constitutively active Rac1 (Rac1V12) accumulate a large central aggregate of membranes beneath the apical membrane that contains filamentous actin, Rac1V12, rab11, and the resident apical membrane protein GP-135 [10].
  • Using Madin-Darby canine kidney cells treated with hepatocyte growth factor/scatter factor or cell lines stably expressing activated v-Src, we show that Rac1 and ARF6 exhibit distinct activation profiles during cell scattering [9].

Associations of RAC1 with chemical compounds

  • We examined roles of the RhoA and Rac1 GTPases in regulating TJ structure and function in MDCK cells using the tetracycline repressible transactivator to regulate RhoAV14, RhoAN19, Rac1V12, and Rac1N17 expression [7].
  • The small guanosine triphosphatase Rac1 is activated by E-cadherin-mediated cell-cell adhesion and is required for the accumulation of actin filaments, E-cadherin, and beta-catenin at sites of cell-cell contact [12].
  • MAP kinase, phosphatidylinositide 3-kinase (PI 3-kinase), and Rac were required downstream of Ras, because loss of adherens junctions was blocked by the inhibitors PD098059 and LY294002 or by dominant-inhibitory mutants of MAP kinase kinase 1 or Rac1 [13].
  • On the other hand, the activation of EP3beta receptor suppressed the elevation of TER and the decrease in paracellular mannitol flux during Ca(2+) switch-induced tight junction formation, whereas the expression of active RhoA or Rac1 did not apparently affect the TER development in the Ca(2+) switch [14].
  • RESULTS: Among the various agents inducing H2O2 generation in dog thyrocytes, carbamylcholine is the only one which activates Rac1, whereas phorbol ester and calcium increase alone have no effect, and cAMP inactivates it [15].


  1. Cdc42 and Rac1 regulate late events in Salmonella typhimurium-induced interleukin-8 secretion from polarized epithelial cells. Hobert, M.E., Sands, K.A., Mrsny, R.J., Madara, J.L. J. Biol. Chem. (2002) [Pubmed]
  2. Cell vacuolation induced by the VacA cytotoxin of Helicobacter pylori is regulated by the Rac1 GTPase. Hotchin, N.A., Cover, T.L., Akhtar, N. J. Biol. Chem. (2000) [Pubmed]
  3. Tachycardia increases NADPH oxidase activity and RyR2 S-glutathionylation in ventricular muscle. Sánchez, G., Pedrozo, Z., Domenech, R.J., Hidalgo, C., Donoso, P. J. Mol. Cell. Cardiol. (2005) [Pubmed]
  4. ARF6-GTP recruits Nm23-H1 to facilitate dynamin-mediated endocytosis during adherens junctions disassembly. Palacios, F., Schweitzer, J.K., Boshans, R.L., D'Souza-Schorey, C. Nat. Cell Biol. (2002) [Pubmed]
  5. Rac1 orientates epithelial apical polarity through effects on basolateral laminin assembly. O'Brien, L.E., Jou, T.S., Pollack, A.L., Zhang, Q., Hansen, S.H., Yurchenco, P., Mostov, K.E. Nat. Cell Biol. (2001) [Pubmed]
  6. Effects of regulated expression of mutant RhoA and Rac1 small GTPases on the development of epithelial (MDCK) cell polarity. Jou, T.S., Nelson, W.J. J. Cell Biol. (1998) [Pubmed]
  7. Structural and functional regulation of tight junctions by RhoA and Rac1 small GTPases. Jou, T.S., Schneeberger, E.E., Nelson, W.J. J. Cell Biol. (1998) [Pubmed]
  8. Rac1 protects epithelial cells against anoikis. Coniglio, S.J., Jou, T.S., Symons, M. J. Biol. Chem. (2001) [Pubmed]
  9. Modulation of Rac1 and ARF6 activation during epithelial cell scattering. Palacios, F., D'Souza-Schorey, C. J. Biol. Chem. (2003) [Pubmed]
  10. Selective alterations in biosynthetic and endocytic protein traffic in Madin-Darby canine kidney epithelial cells expressing mutants of the small GTPase Rac1. Jou, T.S., Leung, S.M., Fung, L.M., Ruiz, W.G., Nelson, W.J., Apodaca, G. Mol. Biol. Cell (2000) [Pubmed]
  11. Ezrin regulates E-cadherin-dependent adherens junction assembly through Rac1 activation. Pujuguet, P., Del Maestro, L., Gautreau, A., Louvard, D., Arpin, M. Mol. Biol. Cell (2003) [Pubmed]
  12. Positive role of IQGAP1, an effector of Rac1, in actin-meshwork formation at sites of cell-cell contact. Noritake, J., Fukata, M., Sato, K., Nakagawa, M., Watanabe, T., Izumi, N., Wang, S., Fukata, Y., Kaibuchi, K. Mol. Biol. Cell (2004) [Pubmed]
  13. Activation of both MAP kinase and phosphatidylinositide 3-kinase by Ras is required for hepatocyte growth factor/scatter factor-induced adherens junction disassembly. Potempa, S., Ridley, A.J. Mol. Biol. Cell (1998) [Pubmed]
  14. Opposite regulation of transepithelial electrical resistance and paracellular permeability by Rho in Madin-Darby canine kidney cells. Hasegawa, H., Fujita, H., Katoh, H., Aoki, J., Nakamura, K., Ichikawa, A., Negishi, M. J. Biol. Chem. (1999) [Pubmed]
  15. Regulation of H2O2 generation in thyroid cells does not involve Rac1 activation. Fortemaison, N., Miot, F., Dumont, J.E., Dremier, S. Eur. J. Endocrinol. (2005) [Pubmed]
WikiGenes - Universities