Journal
IMMUNITY
Volume 12, Issue 4, Pages 419-429Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(00)80194-6
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Funding
- NIGMS NIH HHS [R01 GM061298] Funding Source: Medline
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The death domain kinase RIP and the TNF receptor-associated factor 2 (TRAF2) are essential effecters in TNF signaling. To understand the mechanism by which RIP and TRAF2 regulate TNF-induced activation of the transcription factor NF-KB, we investigated their respective roles in TNF-R1-mediated IKK activation using both RIP-/- and TRAF2(-/-) fibroblasts. We found that TNF-R1-mediated IKK activation requires both RIP and TRAF2 proteins. Although TRAF2 or RIP can be independently recruited to the TNF-R1 complex, neither one of them alone is capable of transducing the TNF signal that leads to IKK activation. Moreover, we demonstrated that IKK is recruited to the TNF-R1 complex through TRAF2 upon TNF treatment and that IKK activation requires the presence of RIP in the same complex.
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