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Published online
doi:10.1083/jcb.200807165
The Journal of Cell Biology, Vol. 182, No. 5, 823-825
The Rockefeller University Press, 0021-9525 $30.00
© McShane et al.
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Survival of the weakest: signaling aided by endosomes



Marisa P. McShane and Marino Zerial

Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany

Correspondence to Marino Zerial: zerial{at}mpi-cbg.de

The tyrosine kinase receptor c-Met plays a key role in cell proliferation, morphogenesis, and motility in response to hepatocyte growth factor. C-Met is often altered in cancer and is a major target for therapeutic intervention. Despite knowing a great deal of the molecular machinery downstream of this receptor tyrosine kinase, the spatiotemporal regulation of c-Met signaling still remains elusive. In this issue of the Journal of Cell Biology, Kermorgant and Parker (Kermorgant, S. and P.J. Parker. 2008. J. Cell Biol. 182:855–863) provide evidence for a model in which the c-Met–activated STAT3 signal is mediated by endosomal trafficking. This study elegantly highlights how weak signals can be effectively transmitted to the nucleus by exploiting endosomal compartments, raising important mechanistic implications for the signaling research community.

© 2008 McShane and Zerial This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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Related Article

Receptor trafficking controls weak signal delivery: a strategy used by c-Met for STAT3 nuclear accumulation
Stéphanie Kermorgant and Peter J. Parker
J. Cell Biol. 2008 182: 855-863. [Abstract] [Full Text] [PDF]





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