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Association of Csk ...
Association of Csk to VE-cadherin and inhibition of cell proliferation
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- Baumeister, Ulf (author)
- Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany
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- Funke, Ruth (author)
- Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany
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- Ebnet, Klaus (author)
- Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany
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- Vorschmitt, Henrik (author)
- Max‐Planck‐Institute of Molecular Biomedicine, Münster, Germany
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- Koch, Stefan (author)
- Max‐Planck‐Institute of Molecular Biomedicine, Münster, Germany
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- Vestweber, Dietmar (author)
- Institute of Cell Biology, ZMBE, University of Münster, Münster, Germany; Max‐Planck‐Institute of Molecular Biomedicine, Münster, Germany
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(creator_code:org_t)
- 2005-04-07
- 2005
- English.
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In: EMBO Journal. - : Wiley-Blackwell Publishing Inc.. - 0261-4189 .- 1460-2075. ; 24:9, s. 1686-1695
- Related links:
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https://europepmc.or...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
Keyword
- Angiogenesis
- Cadherins
- C‐Terminal Src Kinase
- Endothelium
- Proliferation
Publication and Content Type
- ref (subject category)
- art (subject category)
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