The caspase-8 inhibitor FLIP promotes activation of NF-κB and Erk signaling pathways
@article{Kataoka2000TheCI, title={The caspase-8 inhibitor FLIP promotes activation of NF-$\kappa$B and Erk signaling pathways}, author={Takao Kataoka and Ralph C Budd and Nils Holler and Margot Thome and Fabio Martinon and Martin Irmler and Kim Burns and Michael Hahne and Norman J. Kennedy and Magdalena Kovacsovics and Jürg Tschopp}, journal={Current Biology}, year={2000}, volume={10}, pages={640-648} }
596 Citations
NF-κB Signals Induce the Expression of c-FLIP
- BiologyMolecular and Cellular Biology
- 2001
It is shown that NF-κB activation upregulates the caspase 8 inhibitor FLIP, resulting in increased resistance to Fas ligand (FasL) or TNF, and suggest that FLIP is an important mediator of NF-σκB-controlled antiapoptotic signals.
The Fas-associated death domain protein/caspase-8/c-FLIP signaling pathway is involved in TNF-induced activation of ERK.
- Biology, ChemistryExperimental cell research
- 2005
Caspase-8 activity has an essential role in CD95/Fas-mediated MAPK activation
- BiologyCell Death and Disease
- 2011
The combination of biochemical analysis with mathematical modeling provides evidence for an important role of caspase-8 in CD95-mediated activation of MAPKs, while c-FLIP exerts a regulatory function in this process.
Antioxidant c-FLIP Inhibits Fas Ligand-Induced NF-κB Activation in a Phosphatidylinositol 3-Kinase/Akt-Dependent Manner
- BiologyThe Journal of Immunology
- 2011
The presence of two death effector domains of c-FLIP and S-nitrosylation of its caspase-like domain were found to be important for mediating c- FLIP–dependent downregulation of NF-κB activity.
Crosstalk between NF-kappaB-activating and apoptosis-inducing proteins of the TNF-receptor complex.
- Biology, ChemistryMolecular cell biology research communications : MCBRC
- 2001
This review will focus on the crosstalk that exists between proteins of the TNF receptor (TNF-R) signalosome, and which are involved in the initiation of nuclear factor kappa B (NF-kappaB) activation or apoptosis.
Caspase-8 and c-FLIPL Associate in Lipid Rafts with NF-κB Adaptors during T Cell Activation*
- Biology, MedicineJournal of Biological Chemistry
- 2007
A link among TCR, caspases, and the NF-κB pathway that occurs in a sequestered lipid raft environment in T cells is defined.
Regulation of Fas Signaling by FLIP Proteins
- Biology
- 2006
Fas is a member of the tumor necrosis factor receptor family that can induce apoptosis by the recruitment and activation of caspase-8 (formerly called FLICE, MACH or MCH-5). Recently, caspase-8/FLICE…
The c-FLIPL Cleavage Product p43FLIP Promotes Activation of Extracellular Signal-regulated Kinase (ERK), Nuclear Factor κB (NF-κB), and Caspase-8 and T Cell Survival*
- BiologyThe Journal of Biological Chemistry
- 2013
It is demonstrated that acute deletion of endogenous c-FLIP in murine effector T cells results in loss of caspase-8 activity and cell death, which can be rescued by the transgenic expression of p43FLIP, which augments ERK and NF-κB activation, IL-2 production, and T cell proliferation.
MAPK/ERK Overrides the Apoptotic Signaling from Fas, TNF, and TRAIL Receptors*
- BiologyThe Journal of Biological Chemistry
- 2001
The results show that ERK1/2 has a dominant protecting effect over apoptotic signaling from the death receptors, which acts in all cases by suppressing activation of the caspase effector machinery.
Death Receptor-Induced Signaling Pathways Are Differentially Regulated by Gamma Interferon Upstream of Caspase 8 Processing
- BiologyMolecular and Cellular Biology
- 2005
It is shown that IFN-γ sensitizes KB cells for apoptosis induction by facilitating death-inducing signaling complex (DISC)-mediated caspase 8 processing and Fas- and TRAIL death receptor-mediated NF-κB activation leading to synergistic upregulation of a variety of proinflammatory genes.
References
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