作者: H. Y. Song , C. H. Regnier , C. J. Kirschning , D. V. Goeddel , M. Rothe
关键词: MAP kinase kinase kinase 、 Chemistry 、 Kinase 、 TRAF2 、 Cancer research 、 Tumor Necrosis Factor Receptor-Associated Factors 、 Signal transduction 、 TNF receptor associated factor 、 NFKB1 、 c-jun
摘要: TNF-induced activation of the transcription factor NF-κB and c-jun N-terminal kinase (JNK/SAPK) requires TNF receptor-associated 2 (TRAF2). The NF-κB-inducing (NIK) associates with TRAF2 mediates NF-κB. Herein we show that NIK interacts additional members TRAF family this interaction conserved “WKI” motif within domain. We also investigated role in JNK by TNF. Whereas overexpression potently induced activation, it failed to stimulate activation. A kinase-inactive mutant was a dominant negative inhibitor but did not suppress TNF- or TRAF2-induced Thus, is bifurcation point two cascades leading JNK, respectively.