liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Association of Csk to VE-cadherin and inhibition of cell proliferation
Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany.
Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany.
Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany.
Max‐Planck‐Institute of Molecular Biomedicine, Münster, Germany.
Show others and affiliations
2005 (English)In: EMBO Journal, ISSN 0261-4189, E-ISSN 1460-2075, Vol. 24, no 9, p. 1686-1695Article in journal (Refereed) Published
Abstract [en]

Vascular endothelial cadherin (VE-cadherin) mediates contact inhibition of cell growth in quiescent endothelial cell layers. Searching for proteins that could be involved in VE-cadherin signaling, we found the cytosolic C-terminal Src kinase (Csk), a negative regulator of Src family kinases. We show that Csk binds via its SH2 domain to the phosphorylated tyrosine 685 of VE-cadherin. VE-cadherin recruits Csk to cell contacts and both proteins can be co-precipitated from cell lysates of transfected cells and endothelial cells. Association of VE-cadherin and Csk in endothelial cells increased with increasing cell density. CHO cells expressing the tyrosine replacement mutant VE-cadherin-Y685F grow to higher cell densities than cells expressing wild-type VE-cadherin. Overexpression of Csk in these cells under an inducible promoter inhibits cell proliferation in the presence and absence of VE-cadherin, but not in the presence of VE-cadherin-Y685F. Reduction of Csk expression by RNA interference enhances endothelial cell proliferation. Our results suggest that the phosphorylated tyrosine residue 685 of VE-cadherin and probably the binding of Csk to this site are involved in inhibition of cell growth triggered by cell density.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2005. Vol. 24, no 9, p. 1686-1695
Keyword [en]
Angiogenesis, Cadherins, C‐Terminal Src Kinase, Endothelium, Proliferation
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-141650DOI: 10.1038/sj.emboj.7600647ISI: 000228944200005PubMedID: 15861137Scopus ID: 2-s2.0-18944388292ISBN: 0261-4189 (Print) 0261-4189 (Linking) OAI: oai:DiVA.org:liu-141650DiVA: diva2:1149722
Note

Baumeister, Ulf Funke, Ruth Ebnet, Klaus Vorschmitt, Henrik Koch, Stefan Vestweber, Dietmar eng England 2005/04/30 09:00 EMBO J. 2005 May 4;24(9):1686-95. Epub 2005 Apr 7.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records BETA

Koch, Stefan

Search in DiVA

By author/editor
Koch, Stefan
In the same journal
EMBO Journal
Cell and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
isbn
urn-nbn

Altmetric score

doi
pubmed
isbn
urn-nbn
Total: 361 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf