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Nuclear Factor (NF)-κB–regulated X-chromosome–linked iap Gene Expression Protects Endothelial Cells from Tumor Necrosis Factor α–induced Apoptosis

Stehlik, Christian, de Martin, Rainer, Kumabashiri, Ichiro, Schmid, Johannes A., Binder, Bernd R., Lipp, Joachim·1998·The Journal of Experimental Medicine
DOI 10.1084/jem.188.1.211PMC PMC2525542
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Abstract

By differential screening of tumor necrosis factor α (TNF-α) and lipopolysaccharide (LPS)- activated endothelial cells (ECs), we have identified a cDNA clone that turned out to be a member of the inhibitor of apoptosis (iap) gene family. iap genes function to protect cells from undergoing apoptotic death in response to a variety of stimuli. These iap genes, hiap1, hiap2, and xiap were found to be strongly upregulated upon treatment of ECs with the inflammatory cytokines TNF-α, interleukin 1β, and LPS, reagents that lead to activation of the nuclear transcription factor κB (NF-κB). Indeed, overexpression of IκBα, an inhibitor of NF-κB, suppresses the induced expression of iap genes and sensitizes ECs to TNF-α–induced apoptosis. Ectopic expression of one member of the human iap genes, human X-chromosome–linked iap (xiap), using recombinant adenovirus overrules the IκBα effect and protects ECs from TNF-α– induced apoptosis. We conclude that xiap represents one of the NF-κB–regulated genes that counteracts the apoptotic signals caused by TNF-α and thereby prevents ECs from undergoing apoptosis during inflammation.

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Authors
Stehlik, C., de Martin, R., Kumabashiri, I., Schmid, J. A., Binder, B. R., & Lipp, J.
Affiliations
From the Department of Vascular Biology and Thrombosis Research, Vienna International Research and Cooperation Center/University of Vienna, A-1235 Vienna, Austria
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
1998-07-01
Volume
188
Issue
1
Pages
211-216
ISSN
  • 0022-1007
  • 1540-9538
DOI
10.1084/jem.188.1.211
PMC
PMC2525542
Cited by
532
References
1
Language
en

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