2006
DOI: 10.1038/sj.emboj.7601220
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Regulation of antiviral responses by a direct and specific interaction between TRAF3 and Cardif

Abstract: Upon recognition of viral infection, RIG-I and Helicard recruit a newly identified adapter termed Cardif, which induces type I interferon (IFN)-mediated antiviral responses through an unknown mechanism. Here, we demonstrate that TRAF3, like Cardif, is required for type I interferon production in response to intracellular doublestranded RNA. Cardif-mediated IFNa induction occurs through a direct interaction between the TRAF domain of TRAF3 and a TRAF-interaction motif (TIM) within Cardif. Interestingly, while t… Show more

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Cited by 369 publications
(361 citation statements)
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“…In the nucleus, NF-kB and IRF3, as well as other transcription factors and coactivators, collaborate to facilitate the transcription of type I IFN genes. [15][16][17] Complicated virus-host interactions occur during the course of a viral infection. The host cells utilize PRRs to recognize viral components that trigger the induction of type I IFNs and other antiviral genes.…”
Section: Introductionmentioning
confidence: 99%
“…In the nucleus, NF-kB and IRF3, as well as other transcription factors and coactivators, collaborate to facilitate the transcription of type I IFN genes. [15][16][17] Complicated virus-host interactions occur during the course of a viral infection. The host cells utilize PRRs to recognize viral components that trigger the induction of type I IFNs and other antiviral genes.…”
Section: Introductionmentioning
confidence: 99%
“…Functionally, the CARD and TM domains appear to be critical for MAVS dimerization and for relaying the signal from RIG-I to downstream adapter molecules [12,[14][15][16][17]. The Pro region harbors two distinct TIMs, one located at aa 143-PVQET-147 that binds TRAF2 and TRAF3, and a second TIM located at aa 153-PGENSE-158 that exclusively binds TRAF6 [13,18]. An alternate TRAF6-binding site is located in the C-terminus of MAVS at aa 455-PEENEY-460 [13], and both N-and C-terminal sites are required for TRAF6-mediated activation of the NF-κB pathway [13].…”
Section: Introductionmentioning
confidence: 99%
“…We also investigated the effects of TRAF5, which is structurally homologous to TRAF3 [9], on IFN-β expression. As shown in Figure 2 …”
Section: Traf3 and Traf5 Play Roles In Rlr Signaling In Epithelial Cementioning
confidence: 99%
“…Upon viral recognition by RLRs, dimerization of MAVS recruits TNF receptor-associated factors (TRAFs), leading to the activation of transcription factors such as nuclear factor-κB (NF-κB) and interferon regulatory factor (IRF)-3/7. Subsequently, homodimerized IRFs and activated NF-κB translocate from the cytoplasm to the nucleus, resulting in enhanced transcription of pro-inflammatory cytokines and type I interferons (IFNs) [7][8][9][10][11].…”
Section: Introductionmentioning
confidence: 99%
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