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J Biol Chem, Vol. 274, Issue 29, 20139-20143, July 16, 1999

Shc Regulates Epidermal Growth Factor-induced Activation of the JNK Signaling Pathway

Ari HashimotoDagger , Mari KurosakiDagger , Noriko Gotoh§, Masabumi Shibuya§, and Tomohiro KurosakiDagger

From the Dagger  Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570-8506, Japan and the § Department of Genetics, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan

Two adaptor molecules, Grb2 and Shc, have been implicated in the extracellular signal-regulated kinase (ERK) activation by receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR). Here we show that the EGF-mediated ERK activation is abolished by loss of Grb2, whereas this response is not affected by loss of Shc. Conversely, the EGF-mediated c-Jun N-terminal kinase (JNK) activation is dependent on Shc, but not Grb2. These findings strongly support distinct roles for Grb2 and Shc in controlling ERK and JNK activation after EGF stimulation.

Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.


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