โ Scribed by Ernest Hodgson
No coin nor oath required. For personal study only.
Tissue necrosis factor (TNF) induces the production of inflammatory mediators and promotes cell survival through NF-ฮบB and the MAPK pathways. This pathway is an important therapeutic target for inflammatory diseases. We have previously identified that a member of the mitogen-activated kinase kinase kinase family, TAK1, plays essential roles in TNF-signaling pathway leading to activation of NF-ฮบB and MAPKs c-Jun N-terminal kinase (JNK)/p38. We have also identified TAB2 (TAK1-binding protein 2) as a binding partner of TAK1 and have found that TAB2 constitutively associates with TAK1 in culture cells. However, the functional role of TAB2 in TNF signaling has yet to be determined. In this study, we generated and characterized TAB2-deficient fibroblasts by using the Cre-loxP system. Among the TNF-induced cellular events, we found that whole NF-ฮบB pathway, that is, activation of IฮบB kinase (IKK), translocation of NF-ฮบB into the nucleus and DNA binding of NF-ฮบB, was severely
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