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RAC1 — SRF

Text-mined interactions from Literome

Karnoub et al., Mol Cell Biol 2001 (Cell Transformation, Neoplastic) : The insert region of Rac1 was dispensable for Rac1 stimulation of transcription from the cyclin D1 promoter and for activation of the c-Jun, NF-kappaB, and E2F-1 transcription factors but was essential for Rac1 induction of serum response factor activity
Hao et al., EMBO J 2003 : Both SRF and NFAT were also dependent on Rac , Rho, CDC42 and actin
Busche et al., J Cell Sci 2008 : However, using clostridial cytotoxins, we demonstrate that Rac , but not RhoA, is required for SRF and target gene induction in epithelial cells, in contrast to serum stimulated fibroblasts
Benbernou et al., Cell Signal 2013 : We also demonstrated that RhoA and Rock kinases but not Rac were involved in ORs induced SRE/SRF activation and that AP1 was activated, via JNK and p38 MAPKinase
Westwick et al., Mol Cell Biol 1997 (Cell Transformation, Neoplastic) : Surprisingly, PAK binding was dispensable for Rac1 induced transformation and lamellipodium formation, as well as activation of JNK, p38, and serum response factor (SRF) ... Furthermore, Rac1 activation of JNK or SRF , or induction of lamellipodia, was neither necessary nor sufficient for Rac1 transforming activity