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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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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2008
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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. |
format | Text |
id | pubmed-2447904 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT ashwelljonathand tweakingdeath |