NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-09

AUTHORS

O N Ozes, L D Mayo, J A Gustin, S R Pfeffer, L M Pfeffer, D B Donner

ABSTRACT

Activation of the nuclear transcription factor NF-kappaB by inflammatory cytokines requires the successive action of NF-kappaB-inducing kinase (NIK) and an IKB-kinase (IKK) complex composed of IKKalpha and IKKbeta. Here we show that the Akt serine-threonine kinase is involved in the activation of NF-kappaB by tumour necrosis factor (TNF). TNF activates phosphatidylinositol-3-OH kinase (PI(3)K) and its downstream target Akt (protein kinase B). Wortmannin (a PI(3)K inhibitor), dominant-negative PI(3)K or kinase-dead Akt inhibits TNF-mediated NF-kappaB activation. Constitutively active Akt induces NF-kappaB activity and this effect is blocked by dominant-negative NIK. Conversely, NIK activates NF-kappaB and this is blocked by kinase-dead Akt. Thus, both Akt and NIK are necessary for TNF activation of NF-kappaB. Akt mediates IKKalpha phosphorylation at threonine 23. Mutation of this amino acid blocks phosphorylation by Akt or TNF and activation of NF-kappaB. These findings indicate that Akt is part of a signalling pathway that is necessary for inducing key immune and inflammatory responses. More... »

PAGES

82

Journal

TITLE

Nature

ISSUE

6748

VOLUME

401

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/43466

DOI

http://dx.doi.org/10.1038/43466

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1049854869

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10485710


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