IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis.
By Eugene E. Varfolomeev, J. Blankenship, S. Wayson, A. Fedorova, N. Kayagaki, Parie Garg, K. Zobel, Jasmin N. Dynek, L. Elliott, H. Wallweber and 5 more. Cell, 2007
949 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/6afeec19c4b09576a57ca5168e18fbafeec4f9eb
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Citations in the corpus
- Is NF-κB a good target for cancer therapy? Hopes and pitfalls (2009, background): “Within this complex, cIAP1 and cIAP2 are directly responsible for the degradative K48-linked polyubiquitylation of NI”
- Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. (2009, background): “TNF-a and RIPK1 Since Smac mimetic induces apoptosis in certain tumor lines as a result of autocrine TNF-a (Petersen et al., 2007; Vince et al., 2007; Varfolomeev et al., 2007), we checked whether autocrine TNF-a is required for the observed necrosis in HT-29 cells.”
- Life and death by death receptors (2009, background): “In addition to blocking the NF- B transcriptional activity, TNF signaling can also be switched from prosurvival to pro-cell death in transformed cells by simultaneous use of a Smac mimetic, a small molecule designed to resemble the N terminus of Smac that interacts with and inhibits XIAP, cIAP-1, an”
- cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination. (2008, background): “(2007), as these do activate the canonical NF-kB pathway (Gaither et al., 2007; Varfolomeev et al., 2007; Vince et al., 2007).”