JCB logo
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online
doi:10.1083/jcb.200712050
The Journal of Cell Biology, Vol. 182, No. 4, 777-790
The Rockefeller University Press, 0021-9525 $30.00
© Smith et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 4600K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smith, H. W.
Right arrow Articles by Marshall, C. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, H. W.
Right arrow Articles by Marshall, C. J.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Article

uPAR promotes formation of the p130Cas–Crk complex to activate Rac through DOCK180



Harvey W. Smith, Pierfrancesco Marra, and Christopher J. Marshall

Cancer Research UK Centre for Cell and Molecular Biology, Institute of Cancer Research, London SW3 6JB, England, UK

Correspondence to Christopher J. Marshall: Chris.Marshall{at}icr.ac.uk

The urokinase-type plasminogen activator receptor (uPAR) drives tumor cell membrane protrusion and motility through activation of Rac; however, the pathway leading from uPAR to Rac activation has not been described. In this study we identify DOCK180 as the guanine nucleotide exchange factor acting downstream of uPAR. We show that uPAR cooperates with integrin complexes containing β3 integrin to drive formation of the p130Cas–CrkII signaling complex and activation of Rac, resulting in a Rac-driven elongated-mesenchymal morphology, cell motility, and invasion. Our findings identify a signaling pathway underlying the morphological changes and increased cell motility associated with uPAR expression.

Abbreviations used in this paper: ERK, extracellular signal–regulated kinase; GEF, guanine nucleotide exchange factor; GPI, glycosylphosphatidylinositol; HEK, human embryonic kidney; MEK, MAPK/ERK kinase; SD, substrate domain; uPAR, urokinase-type plasminogen activator receptor.

© 2008 Smith et al. 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/).


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents