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- W2474828131 abstract "TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-κB-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-κB-independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders." @default.
- W2474828131 created "2016-07-22" @default.
- W2474828131 creator A5018449456 @default.
- W2474828131 creator A5019205026 @default.
- W2474828131 date "2016-08-01" @default.
- W2474828131 modified "2023-10-16" @default.
- W2474828131 title "More to Life than NF-κB in TNFR1 Signaling" @default.
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- W2474828131 doi "https://doi.org/10.1016/j.it.2016.06.002" @default.
- W2474828131 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5076853" @default.
- W2474828131 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27424290" @default.
- W2474828131 hasPublicationYear "2016" @default.
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