◀ Back to RAC2

RAC2 — ROCK1

Text-mined interactions from Literome

Thirone et al., Am J Physiol Cell Physiol 2009 : Hyperosmolarity provoked cofilin phosphorylation was mediated by the Rho/Rho kinase ( ROCK ) /LIM kinase ( LIMK ) but not the Rac/PAK/LIMK pathway, because 1 ) dominant negative ( DN ) Rho and DN-ROCK but not DN-Rac and DN-PAK inhibited cofilin phosphorylation ; 2 ) constitutively active ( CA ) Rho and CA-ROCK but not CA-Rac and CA-PAK induced cofilin phosphorylation ; 3 ) hyperosmolarity induced LIMK-2 phosphorylation, and 4 ) inhibition of ROCK by Y-27632 suppressed the hypertonicity triggered LIMK-2 and cofilin phosphorylation.We thenexamined whether cofilin and its phosphorylation play a role in the hypertonicity triggered F-actin changes
Hirose et al., J Cell Biol 1998 (Neuroblastoma) : The neurite outgrowth by the p160ROCK inhibition was blocked by coexpression of dominant negative forms of Cdc42 and Rac, indicating that p160ROCK constitutively and negatively regulates neurite formation at least in part by inhibiting activation of Cdc42 and Rac
Tominaga et al., EMBO J 1998 : Expression of a dominant interfering p160ROCK inhibited RhoA-, but not Cdc42- or Rac-activation of NEH1
Zong et al., J Biol Chem 1999 : Rac to Rho point mutations ( V85D or A88D ) within loop 6 of Rac promoted its association with PRK2 and ROCK , whereas the reciprocal Rho ( D87V/D90A ) double mutant significantly reduced effector binding capacity