期刊
FEBS JOURNAL
卷 278, 期 6, 页码 862-876出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1742-4658.2011.08015.x
关键词
apoptosis; caspase 8; IKK necrosis; NF-kappa B; NEMO; RIP1; TNF; TRADD; TRAF2
The molecular mechanisms underlying activation of the I kappa B kinase (IKK) complex are presumably best understood in the context of tumor necrosis factor (TNF) receptor-1 (TNFR1) signaling. In fact, it seems that most, if not all, proteins relevant for this process have been identified and extensive biochemical and genetic data are available for the role of these factors in TNF-induced IKK activation. There is evidence that protein modification-independent assembly of a core TNFR1 signaling complex containing TNFR1-associated death domain, receptor interacting kinase 1, TNF receptor-associated factor 2 and cellular inhibitor of apoptosis protein 1 and 2 starts a chain of nondegrading ubiquitination events that culminate in the recruitment and activation of IKK complex-stimulating kinases and the IKK complex itself. Here, we sum up the known details of TNFR1-induced IKK activation, address arising contradictions and discuss possible explanations resolving the apparent discrepancies.
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