PuSH - Publikationsserver des Helmholtz Zentrums München: Lymphotoxin and lipopolysaccharide induce NF-kappaB-p52 generation by a co-translational mechanism.

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Mordmüller, B.* ; Krappmann, D.* ; Esen, M.* ; Wegener, E.* ; Scheidereit, C.*

Lymphotoxin and lipopolysaccharide induce NF-kappaB-p52 generation by a co-translational mechanism.

EMBO Rep. 4, 82-87 (2003)

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Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.

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The 'classical' NF-kappaB activation pathway proceeds via IkappaB kinase (IKK)-beta/gamma-mediated phosphorylation, induced ubiquitination and the degradation of small IkappaBs. An alternative, NF-kappaB-inducing kinase and IKK-alpha-dependent pathway, which stimulates the processing of NF-kappaB2/p100, has recently been suggested. However, no physiological stimulus has been shown to trigger the activation of this pathway. Here we demonstrate that persistent stimulation with lymphotoxin beta (LT-beta) receptor agonists or lipopolysaccharide (LPS), but not with interleukin-1beta, tumour necrosis factor-alpha or 12-O-tetradecanoylphorbol-13-acetate, induces the generation of p52 DNA-binding complexes by activating the processing of the p100 precursor. Induction of p52 DNA-binding activity is delayed in comparison with p50/p65 complexes and depends on de novo protein synthesis. p100 is constitutively and inducibly polyubiquitinated, and both ubiquitination and p52 generation are coupled to continuing p100 translation. Thus, both LT-beta receptor agonists and LPS induce NF-kappaB/p100 processing to p52 at the level of the ribosome.

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