Published September 18, 1998
| public
Journal Article
Activation of Apoptosis Signal-Regulating Kinase 1 (ASK1) by the Adapter Protein Daxx
Abstract
The Fas death receptor can activate the Jun NH_2-terminal kinase (JNK) pathway through the receptor-associated protein Daxx. Daxx was found to activate the JNK kinase kinase ASK1, and overexpression of a kinase-deficient ASK1 mutant inhibited Fas- and Daxx-induced apoptosis and JNK activation. Fas activation induced Daxx to interact with ASK1, which consequently relieved an inhibitory intramolecular interaction between the amino- and carboxyl-termini of ASK1, activating its kinase activity. The Daxx-ASK1 connection completes a signaling pathway from a cell surface death receptor to kinase cascades that modulate nuclear transcription factors.
Additional Information
© 1998 American Association for the Advancement of Science. 16 March 1998; Accepted 13 August 1998. We are grateful to P. Svec for technical support. We thank S. Nagata, K. Matsumoto, J. Wang, M. J. Lenardo, D. V. Goeddel, M. Goeddert, and Z. Yao for reagents, and A. Hoffmann for valuable advice and critical review of the manuscript. H.I. thanks K. Miyazono for valuable discussion. H.Y.C. is supported by the Medical Scientist Training Program at Harvard Medical School. H.I. is supported by Grants-in-Aid for scientific research from the Ministry of Education, Science, and Culture of Japan. X.Y. is a fellow of the Leukemia Society of America. Supported by NIH grant CA51462.Additional details
- Eprint ID
- 52243
- Resolver ID
- CaltechAUTHORS:20141201-144924408
- Harvard Medical School
- Ministry of Education, Science, and Culture of Japan
- Leukemia Society of America
- CA51462
- NIH
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2014-12-02Created from EPrint's datestamp field
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2021-11-10Created from EPrint's last_modified field