标题
IAPs limit activation of RIP kinases by TNF receptor 1 during development
作者
关键词
-
出版物
EMBO JOURNAL
Volume 31, Issue 7, Pages 1679-1691
出版商
Wiley
发表日期
2012-02-10
DOI
10.1038/emboj.2012.18
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Deletion of cIAP1 and cIAP2 in murine B lymphocytes constitutively activates cell survival pathways and inactivates the germinal center response
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- Tumor Necrosis Factor (TNF) Signaling, but Not TWEAK (TNF-like Weak Inducer of Apoptosis)-triggered cIAP1 (Cellular Inhibitor of Apoptosis Protein 1) Degradation, Requires cIAP1 RING Dimerization and E2 Binding
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- Cellular IAPs inhibit a cryptic CD95-induced cell death by limiting RIP1 kinase recruitment
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- c-IAP1 and c-IAP2 Are Critical Mediators of Tumor Necrosis Factor α (TNFα)-induced NF-κB Activation
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- TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNFα
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- cIAP1 and cIAP2 Facilitate Cancer Cell Survival by Functioning as E3 Ligases that Promote RIP1 Ubiquitination
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- IAPs contain an evolutionarily conserved ubiquitin-binding domain that regulates NF-κB as well as cell survival and oncogenesis
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- Both cIAP1 and cIAP2 regulate TNF -mediated NF- B activation
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