| Literature DB >> 10357816 |
M Grell1, G Zimmermann, E Gottfried, C M Chen, U Grünwald, D C Huang, Y H Wu Lee, H Dürkop, H Engelmann, P Scheurich, H Wajant, A Strasser.
Abstract
Several members of the tumour necrosis factor receptor (TNF-R) superfamily can induce cell death. For TNF-R1, Fas/APO-1, DR3, DR6, TRAIL-R1 and TRAIL-R2, a conserved 'death domain' in the intracellular region couples these receptors to activation of caspases. However, it is not yet known how TNF receptor family members lacking a death domain, such as TNF-R2, CD40, LT-betaR, CD27 or CD30, execute their death-inducing capability. Here we demonstrate in different cellular systems that cytotoxic effects induced by TNF-R2, CD40 and CD30 are mediated by endogenous production of TNF and autotropic or paratropic activation of TNF-R1. In addition, stimulation of TNF-R2 and CD40 synergistically enhances TNF-R1-induced cytotoxicity. These findings describe a novel pro-apoptotic mechanism induced by some members of the TNF-R family.Entities:
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Year: 1999 PMID： 10357816 PMCID： PMC1171385 DOI： 10.1093/emboj/18.11.3034
Source DB: PubMed Journal: EMBO J ISSN： 0261-4189 Impact factor: 11.598