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CFL1 — RHO

Text-mined interactions from Literome

Sumi et al., J Cell Biol 1999 : These results indicate that LIMK2 plays a crucial role both in Rho- and Cdc42 induced actin cytoskeletal reorganization, at least in part by inhibiting the functions of cofilin
Harenberg et al., Eur J Immunol 2005 : TXA ( 2 ) -induced apoptosis of double positive thymocytes and Rho activation required Lsc, and TXA ( 2 ) stimulation of actin polymerization and cofilin phosphorylation required both Lsc and Rho kinase ( ROCK )
Hellstrand et al., Can J Physiol Pharmacol 2005 : Stretch of intact venous smooth muscle activates Rho and inhibits the actin filament severing factor cofilin , resulting in increased actin polymerization
Ball et al., Int J Biochem Cell Biol 2007 : Signaling through platelet derived growth factor receptor-alpha increases smooth muscle alpha-actin filaments by activating RhoA, which results in Rho associated kinase (ROCK) dependent cofilin phosphorylation, enhancing smooth muscle alpha-actin filament polymerization, and also upregulates smooth muscle alpha-actin expression
Lee et al., J Cell Physiol 2008 (Vitreoretinopathy, Proliferative) : TGF-beta1 also increased LIM kinase and cofilin phosphorylation and the Rho inhibitor blocked this effect
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 ... Taken together, cofilin is necessary for maintaining the osmotic responsiveness of the cytoskeleton in tubular cells, and the Rho/ROCK/LIMK mediated cofilin phosphorylation is a key mechanism in the hyperosmotic stress induced F-actin increase
Karlsson et al., Mol Endocrinol 2010 : Basal phosphorylation of cofilin ( Ser3 ) is mediated by active/GTP bound Rho and downstream protein kinases ; LHR signaling promotes a decrease in active/GTP bound Rho by a PKA dependent mechanism ... LHR dependent Rho inactivation and subsequent activation of cofilin does not involve ERK, epidermal growth factor receptor, or phosphatidylinositol 3-kinase pathways downstream of PKA
Kolozsvári et al., Cardiovasc Res 2012 : Exposure of bovine or human pulmonary artery endothelial cells ( BPAECs or HPAECs ) to the CN inhibitor cyclosporin A ( CsA ) induces a rise in intracellular Ca ( 2+ ) and increases the phosphorylation level of cofilin ( Ser3 ) and MYPT1 ( Thr696 ) in a Ca ( 2+ ) -and Rho-kinase dependent manner