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TWEAKing death

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 κB activation, tumor necrosis factor (TNF) α production, TNF receptor 1 occupancy, and caspase-8 activation. In...

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Detalles Bibliográficos
Autor principal: Ashwell, Jonathan D.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447904/
https://www.ncbi.nlm.nih.gov/pubmed/18606854
http://dx.doi.org/10.1083/jcb.200806036
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author Ashwell, Jonathan D.
author_facet Ashwell, Jonathan D.
author_sort Ashwell, Jonathan D.
collection PubMed
description 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 κB activation, tumor necrosis factor (TNF) α 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.
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spelling pubmed-24479042009-01-14 TWEAKing death Ashwell, Jonathan D. J Cell Biol Reviews 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 κB activation, tumor necrosis factor (TNF) α 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. The Rockefeller University Press 2008-07-14 /pmc/articles/PMC2447904/ /pubmed/18606854 http://dx.doi.org/10.1083/jcb.200806036 Text en © 2008 Ashwell This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Reviews
Ashwell, Jonathan D.
TWEAKing death
title TWEAKing death
title_full TWEAKing death
title_fullStr TWEAKing death
title_full_unstemmed TWEAKing death
title_short TWEAKing death
title_sort tweaking death
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447904/
https://www.ncbi.nlm.nih.gov/pubmed/18606854
http://dx.doi.org/10.1083/jcb.200806036
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