TLR3/TICAM-1 signaling in tumor cell RIP3-dependent necroptosis
スポンサーリンク
概要
- 論文の詳細を見る
The engagement of Toll-like receptor 3 (TLR3) leads to the oligomerization of the adaptor TICAM-1 (TRIF), which can induces either of three acute cellular responses, namely, cell survival coupled to Type I interferon production, or cell death, via apoptosis or necrosis. The specific response elicited by TLR3 determines the fate of affected cells, although the switching mechanism between the two cell death pathways in TLR3-stimulated cells remains molecularly unknown. Tumor necrosis factor α (TNFα)-mediated cell death can proceed via apoptosis or via a non-apoptotic pathway, termed necroptosis or programmed necrosis, which have been described in detail. Interestingly, death domain-containing kinases called receptor-interacting protein kinases (RIPs) are involved in the signaling pathways leading to these two cell death pathways. Formation of the RIP1/RIP3 complex (called necrosome) in the absence of caspase 8 activity is crucial for the induction of necroptosis in response to TNFα signaling. On the other hand, RIP1 is known to interact with the C-terminal domain of TICAM-1 and to modulate TLR3 signaling. In macrophages and perhaps tumor cell lines, RIP1/RIP3-mediated necroptotic cell death can ensue the administration of the TLR agonist polyI:C. If this involved the TLR3/TICAM-1 pathway, the innate sensing of viral dsRNA would be linked to cytopathic effects and to persistent inflammation, in turn favoring the release of damage-associated molecular patterns (DAMPs) in the microenvironment. Here, we review accumulating evidence pointing to the involvement of the TLR3/TICAM-1 axis in tumor cell necroptosis and the subsequent release of DAMPs.
- Landes Bioscienceの論文
- 2012-09-00
Landes Bioscience | 論文
- Photosynthesis-dependent Ca2+influx and functional diversity between phospholipases in the formation of cell polarity in migrating cells of red algae
- Effects of cell wall synthesis on cell polarity in the red alga Porphyra yezoensis
- Suppressive Effect of Modified Dominant Negative RAS Mutant on Human Cancer by Gene Transfer with Non-Viral Vector
- Alternative efficacy-predicting markers for paclitaxel instead of CHFR in non-small cell lung cancer
- Protective role of MyD88-independent innate immune responses against prion infection