Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response
- G. OganesyanSupriya K. Saha G. Cheng
- 12 January 2006
Biology, Medicine
It is demonstrated that cells lacking TRAF3, a member of the TNF receptor-associated factor family, are defective in type I IFN responses activated by several different TLRs, suggesting that TRAF 3 serves as a critical link between TLR adaptors and downstream regulatory kinases important for IRF activation.
Regulation of antiviral responses by a direct and specific interaction between TRAF3 and Cardif
- Supriya K. SahaE. Pietras G. Cheng
- 26 July 2006
Biology
It is demonstrated that TRAF3, like Cardif, is required for type I interferon production in response to intracellular double‐stranded RNA, and it is shown that preventing association of TRAf3 with this TIM by mutating two critical amino acids in the TRAF domain also abolishes TRAF 3‐dependent IFN production following viral infection.
The signaling adaptors and pathways activated by TNF superfamily.
- P. DempseyS. DoyleJeannie Q. HeG. Cheng
- 1 June 2003
Biology, Medicine
Activation of noncanonical NF-κB requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2, TRAF3 and the kinase NIK
- B. ZarnegarYaya Wang G. Cheng
- 9 November 2008
Biology
The lethality of TRAF3 deficiency in mice could be rescued by a single NIK gene, highlighting the importance of tightly regulated NIK.
Control of canonical NF-κB activation through the NIK–IKK complex pathway
- B. ZarnegarS. YamazakiJeannie Q. HeG. Cheng
- 4 March 2008
Biology
Evidence that TRAF3 potently suppresses canonical NF-κB activation and gene expression in vitro and in vivo is provided and it is demonstrated that inhibition of TRAf3 results in coordinated activation of both NF-kkB activation pathways.
Downstream regulator TANK binds to the CD40 recognition site on TRAF3.
- Chenglong LiC. Ni K. R. Ely
- 1 March 2002
Biology
Rescue of TRAF3-null mice by p100 NF-κB deficiency
- Jeannie Q. HeB. Zarnegar G. Cheng
- 30 October 2006
Biology, Medicine
Genetic data clearly demonstrate that TRAF3 is a critical negative modulator of the noncanonical NF-κB pathway and that constitutive activation of the other pathway causes the lethal phenotype of TRAf3-deficient mice.
Unique CD40-mediated biological program in B cell activation requires both type 1 and type 2 NF-kappaB activation pathways.
- B. ZarnegarJeannie Q. HeG. OganesyanA. HoffmannD. BaltimoreG. Cheng
- 25 May 2004
Biology
It is suggested that both type 1 and type 2 NF-kappaB pathways contribute to the gene expression and biological program unique for CD40 in B cell activation.
TRAF3 and its biological function.
Tumor necrosis factor receptor associated factor 3 functions as a negative regulator of the NF-kappaB pathway and separately, as a positive regulator of type I IFN production, placing itself as a critical regulator of both innate and adaptive immune responses.
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