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Article: Mediation of TNF receptor-associated factor effector functions by apoptosis signal-regulating kinase-1 (ASK1)

TitleMediation of TNF receptor-associated factor effector functions by apoptosis signal-regulating kinase-1 (ASK1)
Authors
KeywordsDominant negative
Apoptosis
Tumor necrosis factor
Signal transduction
Protein phosphorylation
SAPK/JNK
Protein kinase
Issue Date1999
Citation
Oncogene, 1999, v. 18, n. 42, p. 5814-5820 How to Cite?
AbstractTumor 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 SGPK/JNK activation.
Persistent Identifierhttp://hdl.handle.net/10722/291498
ISSN
2020 Impact Factor: 9.867
2020 SCImago Journal Rankings: 3.395
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHoeflich, Klaus P.-
dc.contributor.authorYeh, Wen Chen-
dc.contributor.authorYao, Zhengbin-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorWoodgett, James R.-
dc.date.accessioned2020-11-17T14:54:30Z-
dc.date.available2020-11-17T14:54:30Z-
dc.date.issued1999-
dc.identifier.citationOncogene, 1999, v. 18, n. 42, p. 5814-5820-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/291498-
dc.description.abstractTumor 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 SGPK/JNK activation.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.subjectDominant negative-
dc.subjectApoptosis-
dc.subjectTumor necrosis factor-
dc.subjectSignal transduction-
dc.subjectProtein phosphorylation-
dc.subjectSAPK/JNK-
dc.subjectProtein kinase-
dc.titleMediation of TNF receptor-associated factor effector functions by apoptosis signal-regulating kinase-1 (ASK1)-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/sj.onc.1202975-
dc.identifier.pmid10523862-
dc.identifier.scopuseid_2-s2.0-0033554554-
dc.identifier.volume18-
dc.identifier.issue42-
dc.identifier.spage5814-
dc.identifier.epage5820-
dc.identifier.isiWOS:000083095100010-
dc.identifier.issnl0950-9232-

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