JCB logo
Marligen Biosciences
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 11 October 2004. doi:10.1083/jcb.200404171
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 1, 171-181
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
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 Beauvais, D. M.
Right arrow Articles by Rapraeger, A. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Beauvais, D. M.
Right arrow Articles by Rapraeger, A. C.
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?

Article

 The syndecan-1 ectodomain regulates {alpha}vß3 integrin activity in human mammary carcinoma cells

DeannaLee M. Beauvais, Brandon J. Burbach, and Alan C. Rapraeger

Department of Pathology and Laboratory Medicine and Program in Molecular and Cellular Pharmacology, University of Wisconsin-Madison, Madison, WI 53706

Correspondence to Alan C. Rapraeger: acraprae{at}wisc.edu

The {alpha}vß3 integrin participates in cell morphogenesis, growth factor signaling, and cell survival. Activation of the integrin is central to these processes and is influenced by specific ECM components, which engage both integrins and syndecans. This paper demonstrates that the {alpha}vß3 integrin and syndecan-1 (S1) are functionally coupled. The integrin is dependent on the syndecan to become activated and to mediate signals required for MDA-MB-231 and MDA-MB-435 human mammary carcinoma cell spreading on vitronectin or S1-specific antibody. Coupling of the syndecan to {alpha}vß3 requires the S1 ectodomain (ED), as ectopic expression of glycosylphosphatidylinositol-linked S1ED enhances {alpha}vß3 recognition of vitronectin; and treatments that target this domain, including competition with recombinant S1ED protein or anti-S1ED antibodies, mutation of the S1ED, or down-regulation of S1 expression by small-interfering RNAs, disrupt {alpha}vß3-dependent cell spreading and migration. Thus, S1 is likely to be a critical regulator of many cellular behaviors that depend on activated {alpha}vß3 integrins.

Abbreviations used in this paper: COL, collagen; ED, ectodomain; FN, fibronectin; GPI, glycosylphosphatidylinositol; Hb, Hepes-buffered; HS, heparan sulfate; hS1, human S1; IMD, integrin-mediated death; LN, laminin; mS1, mouse S1; pAb, polyclonal antibody; S1, syndecan-1; siRNA, small-interfering RNA; TM, transmembrane; VN, vitronectin.


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