Xia Pu, Wang Lijun, Moretti Paul A B, Albanese Nathaniel, Chai Fugui, Pitson Stuart M, D'Andrea Richard J, Gamble Jennifer R, Vadas Mathew A
Division of Human Immunology, The Hanson Institute, Institute of Medical and Veterinary Science and University of Adelaide, Frome Road, Adelaide SA 5000, Australia.
J Biol Chem. 2002 Mar 8;277(10):7996-8003. doi: 10.1074/jbc.M111423200. Epub 2002 Jan 2.
Tumor necrosis factor-alpha (TNF) receptor-associated factor 2 (TRAF2) is one of the major mediators of TNF receptor superfamily transducing TNF signaling to various functional targets, including activation of NF-kappa B, JNK, and antiapoptosis. We investigated how TRAF2 mediates differentially the distinct downstream signals. We now report a novel mechanism of TRAF2-mediated signal transduction revealed by an association of TRAF2 with sphingosine kinase (SphK), a lipid kinase that is responsible for the production of sphingosine 1-phosphate. We identified a TRAF2-binding motif of SphK that mediated the interaction between TRAF2 and SphK resulting in the activation of the enzyme, which in turn is required for TRAF2-mediated activation of NF-kappa B but not JNK. In addition, by using a kinase inactive dominant-negative SphK and a mutant SphK that lacks TRAF2-binding motif we show that the interaction of TRAF2 with SphK and subsequent activation of SphK are critical for prevention of apoptosis during TNF stimulation. These findings show a role for SphK in the signal transduction by TRAF2 specifically leading to activation of NF-kappa B and antiapoptosis.
肿瘤坏死因子-α(TNF)受体相关因子2(TRAF2)是TNF受体超家族的主要介质之一,可将TNF信号转导至各种功能靶点,包括激活核因子κB(NF-κB)、JNK以及抗凋亡作用。我们研究了TRAF2如何差异介导不同的下游信号。我们现在报告一种由TRAF2与鞘氨醇激酶(SphK)结合所揭示的TRAF2介导的信号转导新机制,SphK是一种脂质激酶,负责生成1-磷酸鞘氨醇。我们鉴定出SphK的一个TRAF2结合基序,该基序介导TRAF2与SphK之间的相互作用,从而导致该酶的激活,而这反过来又是TRAF2介导的NF-κB激活而非JNK激活所必需的。此外,通过使用激酶失活的显性负性SphK和缺乏TRAF2结合基序的突变型SphK,我们表明TRAF2与SphK的相互作用以及随后SphK的激活对于TNF刺激期间预防细胞凋亡至关重要。这些发现表明SphK在TRAF2的信号转导中发挥作用,特别是导致NF-κB激活和抗凋亡。