A Small Molecule Smac Mimic Potentiates TRAIL- and TNFα-Mediated Cell Death

By Lin Li, R. Thomas, Hidetaka Suzuki, J. D. De Brabander, Xiaodong Wang, P. Harran. Science, 2004

616 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/22747454dfde4b64491717c72b690eb1b8a81eb0

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Citations in the corpus

Intrinsically disordered proteins in human diseases: introducing the D2 concept. (2008, background): “Structural basis for binding of Smac/DIABLO to the XIAP BIR3 domain.”
Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “Moreover, on the basis of the three-dimensional structure of Smac/ DIABLO in complex with XIAP BIR3, Smac peptidomimetics were designed, which cooperated with TRAIL, TNFa, cisplatin or etoposide to trigger apoptosis in tumor cells (Li et al., 2004; Sun et al., 2004a, b, 2005).”
Role of Bcl-2 family proteins and caspases in the regulation of apoptosis (2011, background): “[228], small molecules [229–235], and peptidic compounds [234, 236, 237] that are under investigation to develop potential therapeutics against IAPs protein which are involved in cancer.”
Is NF-κB a good target for cancer therapy? Hopes and pitfalls (2009, background): “These compounds promote apoptosis of various cancer cells, including multiple myeloma cells, either as single agents or in synergy with other pro-apoptotic stimuli such as TNF&alpha”
The TRAIL apoptotic pathway in cancer onset, progression and therapy (2008, background): “By contrast, small-molecule IAP inhibitors have been developed and these can synergize with TRAIL to induce tumour cell apoptosi”
Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. (2012, positive): “We previously established a robust cell-based model of necrosis by treating human colon cancer HT-29 cells with a combination of TNF-a, a cell-permeable small molecule that mimics Smac function (Smac mimetic), and the pan-caspase inhibitor z-VAD-fmk (He et al., 2009; Li et al., 2004).”
Nonredundant and complementary functions of TRAF2 and TRAF3 in a ubiquitination cascade that activates NIK-dependent alternative NF-κB signaling (2008, background): “Accordingly, Diablo mimics that bind to the same sites on cIAP1 and cIAP2 as does Diablo induce cIAP1 and cIAP2 self-ubiquitination and proteasomal degradation, and stabilization of NI”
Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. (2009, methodology): “Recombinant human TRAIL protein was generated as previously described (Li et al., 2004) and recombinant human FasL was from Axxora.”
IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis. (2007, background): “These results show that IAP antagonists are able to sensitize cells to TNFakillingbyinhibitingcIAP1,andconsequentperturbation of TNF-R1 signaling, and are consistent with reports that IAP antagonists increased sensitivity of HeLa cells to TNFa ( Li et al., 2004 ).”
Autocrine TNFalpha signaling renders human cancer cells susceptible to Smac-mimetic-induced apoptosis. (2007, methodology): “(B) Treatment of selected group of cell lines to 100 nM of compound 3 and to compound 4 (negative control compound with similar structure by differing in function group configuration as described in Li et al., 2004).”
Targeting IAP proteins for therapeutic intervention in cancer (2012, background): “However, a serendipitous discovery of a bivalent SMAC mimetic compound has led to the development of a new class of IAP antagonists and considerably expanded the repertoire of IAP-targeting agent”