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J. Biol. Chem., Vol. 277, Issue 38, 34853-34859, September 20, 2002
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From the Institute of Cell Biology and Immunology, University of
Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
The heat shock protein 90 (Hsp-90) inhibitor,
geldanamycin, and the proteasome inhibitor, MG-132, both inhibited
tumor necrosis factor receptor 1 (TNF-R1)- but not TRAIL-induced
apoptosis in Kym-1 cells, suggesting that TNF-R1-induced cell death is
dependent on NF-
Endogenous Membrane Tumor Necrosis Factor (TNF) Is a Potent
Amplifier of TNF Receptor 1-mediated Apoptosis*
B activation in this model. Triggering of TNF-R1 by
agonistic antibodies led to cell-type specific induction of endogenous
TNF and apoptosis, the latter of which was abrogated by neutralizing TNF specific antibodies. TNF-R1-stimulated cells expressed TNF mainly
in a cell-associated form, suggesting that the endogenously produced
TNF act in its membrane-bound form. Geldanamycin failed to
inhibit apoptosis induction by a combination of agonistic TNF-R1- and
TNF-R2-specific antibodies, indicating that both TNF receptors co-operate in TNF-R1-triggered apoptosis in Kym-1 cells. Thus, TNF-R1
stimulation can elicit a strong and rapid apoptotic response via
induction of membrane TNF and subsequent cooperation of TNF-R1 and
TNF-R2. Moreover, we give evidence that this mechanism circumvents the
need of the prolonged presence of exogenous soluble TNF for TNF-R1-mediated apoptosis induction.
*
This work was supported by Deutsche Forschungsgemeinschaft
Grant Wa 1025/11-1 and Sonderforschungsbereich 495, Project A5.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
49-711-685-7446; Fax: 49-711-685-7484; E-mail:
harald.wajant@po.uni-stuttgart.de.
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