AIP1/DAB2IP, a novel member of the Ras-GAP family, transduces TRAF2-induced ASK1-JNK activation.
作者： Haifeng Zhang , Rong Zhang , Yan Luo , Alessio D'Alessio , Jordan S. Pober
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摘要: Previously we have shown that ASK-interacting protein 1 (AIP1, also known as DAB2IP), a novel member of the Ras-GAP family, mediates TNF-induced activation ASK1-JNK signaling pathway. However, mechanism by which TNF is coupled to AIP1 not known. Here show localized on plasma membrane in resting endothelial cells (EC) complex with TNFR1. binding induces release from TNFR1, resulting cytoplasmic translocation and concomitant formation an intracellular comprised TRADD, RIP1, TRAF2, AIPl. A proline-rich region (amino acids 796–807) critical for maintaining closed form, associates TNFR1 distinct death domain, site association TRADD. An mutant deletion this constitutively binds TRAF2 ASK1. PERIOD-like domain 591–719) intact RING finger specifically enhances TRAF2-induced ASK1 activation. At same time, inhibits IKK-NF-κB signaling. Taken together, our data suggest transducer TRAF2-dependent balance between JNK versus NF-κB
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