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Abstract
The Ras-Raf-MEK [(mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) kinase]-MAPK signaling pathway controls the activation of many cellular functions. Recent reports of Raf-1-deficient mice have indicated that MEK may not be an important downstream substrate for Raf-1 and that, in fact, Raf-1 is important for blocking apoptosis rather than for cell proliferation. Murakami and Morrison examine these recent findings and discuss their implications, as well as other possible conclusions that may be drawn from the published data.
