JCB logo
Quantitative Colocalization Analysis Software
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 3 March 2003. doi:10.1083/jcb.200212114
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 805K)
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 Hsia, D. A.
Right arrow Articles by Schlaepfer, D. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hsia, D. A.
Right arrow Articles by Schlaepfer, D. D.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*OMIM
*UniGene
*Substance via MeSH
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0021-9525/2003/3/753 $5.00
The Journal of Cell Biology, Volume 160, Number 5, 753-767

Article

 Differential regulation of cell motility and invasion by FAK

Datsun A. Hsia1, Satyajit K. Mitra1, Christof R. Hauck1,2, Daniel N. Streblow2, Jay A. Nelson2, Dusko Ilic3, Shuang Huang1, Erguang Li1, Glen R. Nemerow1, Jay Leng1, Kathryn S.R. Spencer1, David A. Cheresh1 and David D. Schlaepfer1

1 Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037
2 Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR 97201
3 Department of Stomatology, University of California, San Francisco, CA 94143

Address correspondence to David D. Schlaepfer, The Scripps Research Institute, Dept. of Immunology, IMM26, 10550 N. Torrey Pines Rd., La Jolla, CA 92037. Tel.: (858) 784-8207. Fax: (858) 784-8227. E-mail: dschlaep{at}scripps.edu

Cell migration and invasion are fundamental components of tumor cell metastasis. Increased focal adhesion kinase (FAK) expression and tyrosine phosphorylation are connected with elevated tumorigenesis. Null mutation of FAK results in embryonic lethality, and FAK-/- fibroblasts exhibit cell migration defects in culture. Here we show that viral Src (v-Src) transformation of FAK-/- cells promotes integrin-stimulated motility equal to stable FAK reexpression. However, FAK-/- v-Src cells were not invasive, and FAK reexpression, Tyr-397 phosphorylation, and FAK kinase activity were required for the generation of an invasive cell phenotype. Cell invasion was linked to transient FAK accumulation at lamellipodia, formation of a FAK–Src-p130Cas–Dock180 signaling complex, elevated Rac and c-Jun NH2-terminal kinase activation, and increased matrix metalloproteinase expression and activity. Our studies support a dual role for FAK in promoting cell motility and invasion through the activation of distinct signaling pathways.

Key Words: motility; invasion; FAK; Src; JNK


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 Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



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