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J Biol Chem, Vol. 274, Issue 9, 5267-5270, February 26, 1999

COMMUNICATION
Requirement of FADD for Tumor Necrosis Factor-induced Activation of Acid Sphingomyelinase

Katja Wiegmann, Ralf Schwandner, Oleg Krut, Wen-Chen Yeh^§, Tak W. Mak^§, and Martin Krönke

From the  Institute of Immunology, University of Kiel, 24105 Kiel, Germany and the ^§ Amgen Institute, University of Toronto and Ontario Cancer Institute, Toronto, Ontario M5G 2M9, Canada

The generation of mice strains deficient for select members of the signaling complex of the 55-kDa tumor necrosis factor receptor (TNF-R55) has allowed the assignment of specific cellular responses to distinct TNF-R55-associated proteins. In particular, the TNF-R55-associated protein FADD seems to be responsible for recruitment and subsequent activation of caspase 8. In this report we demonstrate the requirement of FADD for TNF-induced activation of endosomal acid sphingomyelinase (A-SMase). In primary embryonic fibroblasts from FADD-deficient mice the activation of A-SMase by TNF-R55 ligation was almost completely impaired. This effect is specific in that other TNF responses like activation of NF-B or neutral (N-)SMase remained unaffected. In addition, interleukin-1-induced activation of A-SMase in FADD-deficient cells was unaltered. In FADD^/ embryonic fibroblasts reconstituted by transfection with a FADD cDNA expression construct, the TNF responsiveness of A-SMase was restored. The results of this study suggest that FADD, in addition to its role in triggering a proapoptotic caspase cascade, is required for TNF-induced activation of A-SMase.

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Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.

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