The caspase-8 inhibitor FLIP promotes activation of NF-κB and Erk signaling pathways
By T. Kataoka, R. Budd, N. Holler, M. Thome, Fabio Martinon, M. Irmler, K. Burns, M. Hahne, N. Kennedy, M. Kovacsovics and 1 more. 2000
612 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Pharmacology
View Paper: https://www.semanticscholar.org/paper/5142ade56cc645af3db8ea7392d33a39357a6c9e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
In Molecular Biology
In Pharmacology
Citations in the corpus
- Life and death in peripheral T cells (2007, background): “cFLIP was reported to recruit RAF1 and receptor-interacting protein (RIP), and thereby to activate ERK and NF-κB signalling pathways, respectivel”
- NF-κB Signals Induce the Expression of c-FLIP (2001, background): “We have previously shown that FLIPL, but not FLIPS, binds to TRAF2 and RIP, resulting in strong NF-kB activation upon stimulation of death receptor signaling pathways (12).”
- The CD95(APO-1/Fas) DISC and beyond (2003, background): “One study found that c-FLIP recruited not only TRAF1 and 2 but also RIP and Raf-1, which activated the extracellular signal regulated kinase (Erk) pathway.(41)”
- Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule (2000, background): “Next we examined whether other proteins that are described as components of the Fas DISC, such as RI”