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TRADD–TRAF2 and TRADD–FADD Interactions Define Two Distinct TNF Receptor 1 Signal Transduction Pathways
TLDR
It is shown that TRADD directly interacts with TRAF2 and FADD, signal transducers that activate NF-kappa B and induce apoptosis, respectively, and these two TNFR1-TRADD signaling cascades appear to bifurcate at TRADD.
VISA is an adapter protein required for virus-triggered IFN-beta signaling.
TLDR
Depletion of VISA inhibits virus-triggered and RIG-I-mediated activation of IRF-3, NF-kappaB, and the IFN-beta promoter, suggesting that VISA plays a central role in virus- Triggered TLR3-independent IFn-beta signaling.
TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex.
TLDR
It is shown that TRADD interacts strongly with RIP, another death domain protein that was shown previously to associate with Fas antigen, and is a serine-threonine kinase that is recruited by TRADD to TNFR1 in a TNF-dependent process.
The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation.
TLDR
The results suggest that MITA is a critical mediator of virus-triggered IRF3 activation and IFN expression and further demonstrate the importance of certain mitochondrial proteins in innate antiviral immunity.
VISA Is an Adapter Protein Required for Virus-Triggered IFN-β Signaling
TLDR
Depletion of VISA inhibits virus-triggered and RIG-I-mediated activation of IRF-3, NF-kappaB, and the IFN-beta promoter, suggesting that VISA plays a central role in virus- Triggered TLR3-independent IFn-beta signaling.
FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis.
TLDR
CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did.
The tumor necrosis factor receptor 2 signal transducers TRAF2 and c-IAP1 are components of the tumor necrosis factor receptor 1 signaling complex.
TLDR
The physiological involvement of TRAF2 and c-IAP1 in TNF-R1 signaling is established and a molecular explanation for both the overlapping and distinct signals generated by the two TNF receptors is provided.
Reduced competitiveness of autoantigen-engaged B cells due to increased dependence on BAFF.
TLDR
It is demonstrated that under conditions where BAFF levels are elevated, autoantigen-engaged cells will be rescued from rapid competitive elimination, predisposing to the development of autoimmune disease.
Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development.
TLDR
It is suggested that Casper has two distinct roles: to cooperate with FADD and caspase-8 during embryonic development and to mediate cytoprotection against death factor-induced apoptosis.
I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction.
TLDR
Overexpression of I-TRAF inhibits TRAF2-mediated NF-kappa B activation signaled by CD40 and both TNF receptors, and appears as a natural regulator of TRAF function that may act by maintaining TRAFs in a latent state.
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