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CARP2 deficiency does not alter induction of NF-κB by TNFα

Abstract : TNFα can activate pathways leading to caspase-8-mediated apoptosis, as well as inflammatory pathways signaled by transcription factors. The adaptor protein RIP1 is a critical component for TNF receptor 1 (TNFR1)-mediated activation of NF-κB, because deletion of the gene encoding RIP1 in mice prevents induction of NF-κB by TNFα and causes severe runting with early postnatal lethality [1]. Recently, it has been proposed that caspase 8 and 10 associated RING protein-2 (CARP2, also named RIFIFYLIN/SAKURA) binds to the TNFR1 complex, leading to ubiquitylation and proteasome-mediated degradation of RIP1, thereby limiting the level of NF-κB activated by TNFα [2]. However, our experiments in mice lacking the Rififylin/Carp2 gene question this conclusion, because levels of RIP1 and induction of NF-κB by TNFα are normal in the absence of CARP2.
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Contributor : Michel Cohen-Tannoudji Connect in order to contact the contributor
Submitted on : Thursday, March 21, 2019 - 2:32:50 PM
Last modification on : Thursday, April 7, 2022 - 10:10:25 AM

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Afsar Ahmed, Maryline Moulin, Franck Coumailleau, W Wei-Lynn Wong, Maria Miasari, et al.. CARP2 deficiency does not alter induction of NF-κB by TNFα. Current Biology - CB, Elsevier, 2009, 19 (1), pp.R15-R17. ⟨10.1016/j.cub.2008.11.040⟩. ⟨pasteur-02075501⟩



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