Cell
Volume 87, Issue 3, 1 November 1996, Pages 565-576
Journal home page for Cell

Article
Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-κB Activation Prevents Cell Death

https://doi.org/10.1016/S0092-8674(00)81375-6Get rights and content
Under an Elsevier user license
open archive

Abstract

Through its type 1 receptor (TNFR1), the cytokine TNF elicits an unusually wide range of biological responses, including inflammation, tumor necrosis, cell proliferation, differentiation, and apoptosis. We investigated how TNFR1 activates different effector functions; the protein kinase JNK, transcription factor NF-κB, and apoptosis. We found that the three responses are mediated through separate pathways. Recruitment of the signal transducer FADD to the TNFR1 complex mediates apoptosis but not NF-κB or JNK activation. Two other signal transducers, RIP and TRAF2, mediate both JNK and NF-κB activation. These two responses, however, diverge downstream to TRAF2. Most importantly, JNK activation is not involved in induction of apoptosis, while activation of NF-κB protects against TNF-induced apoptosis.

Cited by (0)