Deconstructing ERK Signaling in Tumorigenesis

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Deconstructing ERK Signaling in Tumorigenesis Patricia G. Santamaria, Angel R. Nebreda  Molecular Cell  Volume 38, Issue 1, Pages 3-5 (April 2010) DOI: 10.1016/j.molcel.2010.03.012 Copyright © 2010 Elsevier Inc. Terms and Conditions

Figure 1 Regulation of Ras-Induced EMT by ERK2 Binding of Ras to GTP in response to growth factor stimulation leads to the activation of the ERK1/2 kinase cascade. Recruitment of substrates containing D- or DEF domains branches out ERK1/2 signaling to specific targets (inset). ERK2 induces EMT by recruiting Fra1 via DEF motif interactions, leading to Fra1 upregulation, which in turn triggers the accumulation of ZEB1/2, critical inducers of the EMT program. Additional mechanisms are likely to be involved in Ras-induced EMT, cell migration, and invasion, for example through the activation of RSK1/2. Molecular Cell 2010 38, 3-5DOI: (10.1016/j.molcel.2010.03.012) Copyright © 2010 Elsevier Inc. Terms and Conditions