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.
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Dates
Type | When |
---|---|
Created | 23 years, 1 month ago (July 27, 2002, 5:37 a.m.) |
Deposited | 1 year, 7 months ago (Jan. 12, 2024, 10:27 p.m.) |
Indexed | 2 weeks, 3 days ago (Aug. 12, 2025, 5:53 p.m.) |
Issued | 26 years, 11 months ago (Sept. 18, 1998) |
Published | 26 years, 11 months ago (Sept. 18, 1998) |
Published Print | 26 years, 11 months ago (Sept. 18, 1998) |
@article{Chang_1998, title={Activation of Apoptosis Signal-Regulating Kinase 1 (ASK1) by the Adapter Protein Daxx}, volume={281}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.281.5384.1860}, DOI={10.1126/science.281.5384.1860}, number={5384}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Chang, Howard Y. and Nishitoh, Hideki and Yang, Xiaolu and Ichijo, Hidenori and Baltimore, David}, year={1998}, month=sep, pages={1860–1863} }