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Sci. STKE, 11 September 2001
Vol. 2001, Issue 99, p. pe30
[DOI: 10.1126/stke.2001.99.pe30]

PERSPECTIVES

Raf-1 Without MEK?

Monica S. Murakami, and Deborah K. Morrison

The authors are at the Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA. E-mail: morrisod{at}nciaxp.ncifcrf.gov

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.

Citation:
M. S. Murakami, D. K. Morrison, Raf-1 Without MEK?. Science's STKE (2001), http://stke.sciencemag.org/cgi/content/full/OC_sigtrans;2001/99/pe30.

© 2001 American Association for the Advancement of Science

Citation: M. S. Murakami, D. K. Morrison, Raf-1 Without MEK? Sci. STKE 2001, pe30 (2001).

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