Publication Date:
1998-09-22
Description:
The Fas death receptor can activate the Jun NH2-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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, H Y -- Nishitoh, H -- Yang, X -- Ichijo, H -- Baltimore, D -- CA51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1860-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743501" target="_blank"〉PubMed〈/a〉
Keywords:
Adaptor Proteins, Signal Transducing
;
Alleles
;
Amino Acid Sequence
;
Animals
;
Antigens, CD95/metabolism
;
*Apoptosis
;
Calcium-Calmodulin-Dependent Protein Kinases/metabolism
;
Carrier Proteins/*metabolism
;
Cell Line
;
Enzyme Activation
;
Humans
;
*Intracellular Signaling Peptides and Proteins
;
JNK Mitogen-Activated Protein Kinases
;
MAP Kinase Kinase Kinases
;
*Mitogen-Activated Protein Kinases
;
Molecular Sequence Data
;
*Nuclear Proteins
;
Protein-Serine-Threonine Kinases/genetics/*metabolism
;
Recombinant Fusion Proteins/metabolism
;
Signal Transduction
;
Tumor Cells, Cultured
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
