Cross-cascade activation of ERKs and ternary complex factors by Rho family proteins

摘要: Mitogens promote cell growth through integrated signal transduction networks that alter cellular metabolism, gene expression and cytoskeletal organization. Many such signals are propagated activation of MAP kinase cascades partly regulated by upstream small GTP-binding proteins. Interactions among suspected but not defined. Here we show Rho family G proteins as Rac1 Cdc42hs, which activate the JNK/SAPK pathway, cooperate with Raf-1 to ERK pathway. This causes ternary complex factors (TCFs), regulate c-fos serum response element. Examination pathway kinases shows neither MEK1 nor Ras will synergize Rho-type proteins, only is fully activated, indicating MEKs a focal point for cross-cascade regulation. utilize PAKs this effect, an active PAK1 mutant can substitute interfering blocks protein stimulation ERKs. phosphorylates on Ser298, site important binding in vivo. Expression also reduces TCF function factors, while enhances EGF-stimulated activity. demonstrates interaction elements previously recognized suggests explanation cooperative effect transformation.