NF-κB Signals Induce the Expression of c-FLIP

By O. Micheau, S. Lens, O. Gaide, K. Alevizopoulos, J. Tschopp. Molecular and Cellular Biology, 2001

795 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e5c76eeb87ec2611f5882d541380d240f1ac8b34

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

1. S. Ghosh
2. M. Hayden
3. M. Karin
4. Junying Yuan
5. D. Ofengeim
6. V. Dixit
7. K. Newton
8. U. Siebenlist

In Molecular Biology

1. Douglas R. Green
2. Junying Yuan
3. M. Karin
4. M. Hayden
5. V. Dixit
6. S. Ghosh
7. A. Strasser
8. D. Ofengeim

In Oncology

1. M. Hayden
2. M. Karin
3. S. Ghosh
4. Junying Yuan
5. D. Ofengeim
6. Douglas R. Green
7. O. Micheau
8. A. Strasser

Citations in the corpus

• Constitutive Nuclear Factor κB Activity Is Required for Survival of Activated B Cell–like Diffuse Large B Cell Lymphoma Cells (2001, background): “1864 NF- B Activity in Subtypes of Diffuse Large B Cell Lymphoma [34], IRF-4 [13], c-FLIP [35], BCL-2 [7, 36], CCR7 [36], and I B [37, 38]) were highly expressed in many of the ABC DLBCLs and tended to be poorly expressed in GCB DLBCLs.”
• Nuclear factor-κB in cancer development and progression (2006, background): “Such interventions were found to inhibit the expression of several critical anti-apoptotic proteins, including the specific inhibitor of caspase 8 activation c-FLI”
• TNF‐mediated inflammatory disease (2008, background): “The recruitment and activation of procaspase 8 can be inhibited by cFLIP, and elevated levels of cFLIP induced by NF-κB activation may prevent the activation of this death pathway [30].”
• NF-κB, the first quarter-century: remarkable progress and outstanding questions. (2012, background): “Ligation of TNFR1 by TNF results in the formation of a proinflammatory, multisubunit signaling structure, termed complex I (Micheau et al. 2001), in which TRAF2 is a key component.”
• A guide to cell death pathways (2023, positive): “In living cells, correctly assembled and ubiquitylated complex I is crucial for the activation of canonical NF-κB, a pro-survival and pro-inflammatory transcriptional pathway that controls the expression of CFLAR and TNFAIP3 , which encode key regulators of apoptosis and inflammation 43–46 .”
• Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes. (2003, positive): “TNFR1 triggers apoptosis in the NF-B unresponsive HT1080 I-kBmut cells NF-B can promote the expression of several anti-apoptotic genes such as TRAF1, TRAF2, cIAP-1, c-IAP-2 and notably FLIPL, a potent inhibitor of death receptorinduced apoptosis (Micheau et al., 2001; Wang et al., 1998).”
• NF-kB in development and progression of human cancer (2005, background): “[35, 41 ]. FLIP shares a high degree of homology with caspase-8 but lacks protease activity and competes with caspase-8 for the binding to the Death-Inducing Signaling Complex (DISC).”
• Signaling in innate immunity and inflammation. (2012, background): “Because expression of c-FLIP is driven by NF-kB (Micheau et al. 2001) and many viruses have evolved strategies to inhibit NF-kB activation (Shisler and Jin 2004; Taylor et al.”