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Deconstructing ERK Signaling in Tumorigenesis

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Presentation on theme: "Deconstructing ERK Signaling in Tumorigenesis"— Presentation transcript:

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

2 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  , 3-5DOI: ( /j.molcel ) Copyright © 2010 Elsevier Inc. Terms and Conditions


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