作者: You Cheng Xu , Ru Feng Wu , Ying Gu , Yih-Sheng Yang , Meng-Chun Yang
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摘要: We previously found that the angiogenic factors TNFα and HIV-1 Tat activate an NAD(P)H oxidase in endothelial cells, which operates upstream of c-Jun N-terminal kinase (JNK), a MAPK involved determination cell fate. To further understand oxidant-related signaling pathways, we screened lung libraries for interaction partners p47 phox recovered orphan adapter TNF receptor-associated factor 4 (TRAF4). Domain analysis suggested tail-to-tail between C terminus conserved TRAF domain TRAF4. In addition, TRAF4, like , was largely cytoskeleton/membrane fraction. Coexpression TRAF4 increased oxidant production JNK activation, whereas each alone had minimal effect. fusion constitutively activated JNK, this activation decreased by antioxidant N-acetyl cysteine. contrast, overexpression binding blocked Tat, suggesting uncoupling from events. A secondary screen proteins TRAF4-interacting yielded number known to control conclude agonists such as initiate signals enter basic cassettes at level oxidase. speculate cells may target endogenous specific sites critical cytokine mechanism increasing signal specificity decreasing toxicity these reactive species.