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LIMK1 — RAC1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Stanyon et al., Int J Biochem Cell Biol 1999
(Williams Syndrome) :
Rac-GTP
enhances phosphorylation of
LIMK1 and cofilin, which leads to accumulation of F-actin, while
Rac-GDP and PMA reduce these effects
Sumi et al., J Biol Chem 2001
:
Activation of LIMK2 by RhoA was inhibited by Y-27632, a specific inhibitor of ROCK, but
Rac1 mediated activation of
LIMK1 was not
Nishita et al., Mol Cell Biol 2002
:
Expression of dominant negative Rac (
DN-Rac ), but not DN-Rho or DN-Cdc42,
blocked SDF-1alpha induced activation of
LIMK1 , which means that SDF-1alpha induced LIMK1 activation is mediated by Rac but not by Rho or Cdc42
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
Huang et al., Biochem Biophys Res Commun 2012
(Vitreoretinopathy, Proliferative) :
Vitreous treatment also enhanced the phosphorylation of
LIMK1 and cofilin and the
Rac inhibitor
blocked this effect
Yang et al., Nature 1998
:
Furthermore, insulin and an active form of
Rac increase the activity of
LIMK-1