Mediation of TNF receptor-associated factor effector functions by apoptosis signal-regulating kinase-1 (ASK1) View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-10-13

AUTHORS

Klaus P Hoeflich, Wen-Chen Yeh, Zhengbin Yao, Tak W Mak, James R Woodgett

ABSTRACT

Tumor necrosis factor-α (TNF), a major inflammatory cytokine, generates a wide variety of cellular responses via key cytoplasmic adaptor molecules named TNF receptor-associated factors (TRAFs). We report that TRAF2, TRAF5 and TRAF6 associate with apoptosis signal-regulating kinase 1 (ASK1), and a catalytically-inactive ASK1 mutant blocks stress-activated protein kinase (SAPK)/Jun NH2-terminal kinase (JNK) activation by these TRAFs. A truncated derivative of TRAF2, which inhibits SAPK activation by TNF, blocks TNF-induced ASK1 activation. Furthermore, protection from TNF-induced cell death conferred by an ASK1 mutant is dependent upon TRAF2. Hence, ASK1 is a common mediator of TRAF-regulated SAPK and apoptosis signaling, and the TRAF2 – ASK1 connection completes the signaling cascade from TNF to SAPK/JNK activation. More... »

PAGES

5814-5820

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1202975

DOI

http://dx.doi.org/10.1038/sj.onc.1202975

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1014288912

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10523862


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