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Gene Review

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

Gallus gallus

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Disease relevance of RAC1


High impact information on RAC1

  • We conclude that rac1 is required for the adhesive and motile function of growth cones rather than the assembly of neurites per se [2].
  • Expression of a dominant negative form of rac1 inhibits spontaneous, growth cone-mediated neurite elongation in response to NGF, but does not substantially affect tension-induced neurite elongation [2].
  • Stable expression of EGFP-K-Ras (V12) down-regulated the activity of Rac1 and RhoA, resulting in reduced subcortical actin filaments and stress fibers, which might contribute to the epithelial dedifferentiation [3].
  • Rac1-dependent actin filament organization in growth cones is necessary for beta1-integrin-mediated advance but not for growth on poly-D-lysine [4].
  • In contrast, on poly-D-lysine, neither Rac1 mutant affected growth cone advance, neurite outgrowth, or neurite differentiation despite inducing similar changes in the amount of rhodamine-phalloidin staining in growth cones [4].

Anatomical context of RAC1


Analytical, diagnostic and therapeutic context of RAC1

  • Immunohistochemistry was used to determine the distribution of Rac1, Cdc42, RhoA and RhoB GTPases during development of the chick retina [1].


  1. Distribution of the small molecular weight GTP-binding proteins Rac1, Cdc42, RhoA and RhoB in the developing chick retina. Santos-Bredariol, A.S., Santos, M.F., Hamassaki-Britto, D.E. J. Neurocytol. (2002) [Pubmed]
  2. Rac is required for growth cone function but not neurite assembly. Lamoureux, P., Altun-Gultekin, Z.F., Lin, C., Wagner, J.A., Heidemann, S.R. J. Cell. Sci. (1997) [Pubmed]
  3. Oncogenic K-Ras down-regulates Rac1 and RhoA activity and enhances migration and invasion of pancreatic carcinoma cells through activation of p38. Dreissigacker, U., Mueller, M.S., Unger, M., Siegert, P., Genze, F., Gierschik, P., Giehl, K. Cell. Signal. (2006) [Pubmed]
  4. Rac1-dependent actin filament organization in growth cones is necessary for beta1-integrin-mediated advance but not for growth on poly-D-lysine. Kuhn, T.B., Brown, M.D., Bamburg, J.R. J. Neurobiol. (1998) [Pubmed]
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