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Published online July 7, 2008
doi:10.1083/jcb.200806036
The Journal of Cell Biology, Vol. 182, No. 1, 15-17
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Ashwell
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 TWEAKing death

Jonathan D. Ashwell

Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892

Correspondence to Jonathan Ashwell: jda{at}pop.nci.nih.gov

Smac mimetics (inhibitor of apoptosis [IAP] antagonists) are synthetic reagents that kill susceptible tumor cells by inducing degradation of cellular IAP (cIAP) 1 and cIAP2, nuclear factor {kappa}B activation, tumor necrosis factor (TNF) {alpha} production, TNF receptor 1 occupancy, and caspase-8 activation. In this issue of The Journal of Cell Biology, Vince et al. (see p. 171) report remarkable similarities in the events leading to tumor cell death triggered by the cytokine TWEAK (TNF-like weak inducer of apoptosis) and IAP antagonists. Although the mechanistic details differ, a common and necessary feature that is also shared by TNF receptor 2 signaling is reduction in the level of cIAP1 and, in some cases, cIAP2 and TNF receptor-associated factor 2. These findings not only extend our appreciation of how cell death pathways are kept in check in tumors, they reinforce the possible utility of induced cIDE (cIAP deficiency) in the selective elimination of neoplastic cells.

Abbreviations used in this paper: cIAP, cellular inhibitors of apoptosis; cIDE, cIAP deficiency; TNFRSF, TNF receptor superfamily; TRAF2, TNF receptor-associated factor 2; TWEAK, TNF-like weak inducer of apoptosis.


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TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNF{alpha}
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