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Current Biology : CB|March 21, 1998
Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL-R/Apo2-mediated cell death but not gene inductionH Wajant, F J Johannes, E Haas, et al.
Cell Death and Differentiation|July 30, 2005
Restoration of membrane TNF-like activity by cell surface targeting and matrix metalloproteinase-mediated processing of a TNF prodrugJ Gerspach, D Müller, S Münkel, et al.
The Journal of Biological Chemistry|June 1, 2001
Fas-associated death domain protein (FADD) and caspase-8 mediate up-regulation of c-Fos by Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via a FLICE inhibitory protein (FLIP)-regulated pathwayD Siegmund, D Mauri, N Peters, et al.
Oncogene|June 6, 2006
TRAIL promotes metastasis of human pancreatic ductal adenocarcinomaA Trauzold, D Siegmund, B Schniewind, et al.
Cell Death and Differentiation|June 27, 2009
TNF-like weak inducer of apoptosis inhibits proinflammatory TNF receptor-1 signalingA Wicovsky, S Salzmann, C Roos, et al.
Cell Death and Differentiation|April 10, 2010
Mutant PIK3CA licenses TRAIL and CD95L to induce non-apoptotic caspase-8-mediated ROCK activationM Ehrenschwender, D Siegmund, A Wicovsky, et al.
The Journal of Biological Chemistry|May 16, 2000
The tumor necrosis factor-related apoptosis-inducing ligand receptors TRAIL-R1 and TRAIL-R2 have distinct cross-linking requirements for initiation of apoptosis and are non-redundant in JNK activationF Mühlenbeck, P Schneider, J L Bodmer, et al.
Cell|December 1, 1995
The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptorM Grell, E Douni, H Wajant, et al.
The EMBO Journal|June 5, 1999
Induction of cell death by tumour necrosis factor (TNF) receptor 2, CD40 and CD30: a role for TNF-R1 activation by endogenous membrane-anchored TNFM Grell, G Zimmermann, E Gottfried, et al.
Oncogene|October 13, 2000
Caspase-8/FLICE functions as an executioner caspase in anticancer drug-induced apoptosisI H Engels, A Stepczynska, C Stroh, et al.
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