Regulation of RIP1 kinase signalling at the crossroads of inflammation and cell death
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Molecular Biology
Link
http://www.nature.com/articles/nrm3683.pdf
Reference96 articles.
1. Stanger, B. Z., Leder, P., Lee, T. H., Kim, E. & Seed, B. RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death. Cell 81, 513–523 (1995).
2. Ting, A. T., Pimentel-Muinos, F. X. & Seed, B. RIP mediates tumor necrosis factor receptor 1 activation of NF-κB but not Fas/APO-1-initiated apoptosis. EMBO J. 15, 6189–6196 (1996). Shows the crucial role of RIP1 in mediating NF-κB activation downstream of TNFR1.
3. Christofferson, D. E. et al. A novel role for RIP1 kinase in mediating TNFα production. Cell Death Dis. 3, e320 (2012).
4. Degterev, A. et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. Nature Chem. Biol. 4, 313–321 (2008). Demonstrates that RIP1 kinase is the target of necrostatin 1.
5. Holler, N. et al. Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nature Immunol. 1, 489–495 (2000). The first paper showing a crucial role of RIP1 kinase in mediating necrotic cell death in Jurkat T cells activated by FAS.
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