NIK promotes tissue destruction independently of the alternative NF-κB pathway through TNFR1/RIP1-induced apoptosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

L Boutaffala, M J M Bertrand, C Remouchamps, G Seleznik, F Reisinger, M Janas, C Bénézech, M T Fernandes, S Marchetti, F Mair, C Ganeff, A Hupalowska, J-E Ricci, B Becher, J Piette, P Knolle, J Caamano, P Vandenabeele, M Heikenwalder, E Dejardin

ABSTRACT

NF-κB-inducing kinase (NIK) is well-known for its role in promoting p100/NF-κB2 processing into p52, a process defined as the alternative, or non-canonical, NF-κB pathway. Here we reveal an unexpected new role of NIK in TNFR1-mediated RIP1-dependent apoptosis, a consequence of TNFR1 activation observed in c-IAP1/2-depleted conditions. We show that NIK stabilization, obtained by activation of the non-death TNFRs Fn14 or LTβR, is required for TNFα-mediated apoptosis. These apoptotic stimuli trigger the depletion of c-IAP1/2, the phosphorylation of RIP1 and the RIP1 kinase-dependent assembly of the RIP1/FADD/caspase-8 complex. In the absence of NIK, the phosphorylation of RIP1 and the formation of RIP1/FADD/caspase-8 complex are compromised while c-IAP1/2 depletion is unaffected. In vitro kinase assays revealed that recombinant RIP1 is a bona fide substrate of NIK. In vivo, we demonstrated the requirement of NIK pro-death function, but not the processing of its substrate p100 into p52, in a mouse model of TNFR1/LTβR-induced thymus involution. In addition, we also highlight a role for NIK in hepatocyte apoptosis in a mouse model of virus-induced TNFR1/RIP1-dependent liver damage. We conclude that NIK not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1/RIP1-dependent cell death independently of the alternative NF-κB pathway. More... »

PAGES

2020-2033

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/cdd.2015.69

    DOI

    http://dx.doi.org/10.1038/cdd.2015.69

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1031097128

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26045047


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