TRAF2 is essential for JNK but not NF-kappa B activation and regulates lymphocyte proliferation and survival
TRAF2 is essential for JNK but not NF-kappa B activation and regulates lymphocyte proliferation and survival
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DOI：
10.1016/s1074-7613(00)80390-8
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发表时间：
1997-11-01
期刊：
影响因子：
32.4
通讯作者：
Choi, Y
中科院分区：
文献类型：
--
作者：
Lee, SY;Reichlin, A;Choi, Y
据信，TRAF2介导由肿瘤坏死因子受体（TNFR）超家族诱导的NF -κB和JNK的活化，肿瘤坏死因子受体超家族在淋巴细胞中引发多效性反应。我们通过表达一种淋巴细胞特异性的TRAF2显性负性形式来研究TRAF2在这些过程中的生理作用，从而阻断该蛋白的效应功能。我们发现，TNFR超家族信号激活JNK需要TRAF2，但激活NF -κB不需要。此外，我们表明在TNF诱导的细胞凋亡过程中，TRAF2诱导不依赖NF -κB的抗凋亡途径。抑制TRAF2会导致脾肿大、淋巴结病以及B细胞数量增加。这些发现表明，TRAF2在体内参与淋巴细胞功能和生长的调节。
TRAF2 is believed to mediate the activation of NF-kappa B and JNK induced by the tumor necrosis factor receptor (TNFR) superfamily, which elicits pleiotropic responses in lymphocytes. We have investigated the physiological roles of TRAF2 in these processes by expressing a lymphocyte-specific dominant negative form of TRAF2, thereby blocking this protein's effector function. We find that the TNFR superfamily signals require TRAF2 for activation of JNK but not NF-kappa B. In addition, we show that TRAF2 induces NF-kappa B-independent anti-apoptotic pathways during TNF-induced apoptosis. Inhibition of TRAF2 leads to splenomegaly, lymphadenopathy, and an increased number of B cells. These findings indicate that TRAF2 is involved in the regulation of lymphocyte function and growth in vivo.