FADD/MORT1的显性干扰突变体增强自身反应性胸腺细胞的缺失并抑制成熟T淋巴细胞的增殖。
A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes.
作者信息
Newton K, Harris A W, Bath M L, Smith K G, Strasser A
机构信息
The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Melbourne, Victoria 3050, Australia.
出版信息
EMBO J. 1998 Feb 2;17(3):706-18. doi: 10.1093/emboj/17.3.706.
Abstract
Members of the tumour necrosis factor receptor family that contain a death domain have pleiotropic activities. They induce apoptosis via interaction with intracellular FADD/MORT1 and trigger cell growth or differentiation via TRADD and TRAF molecules. The impact of FADD/MORT1-transduced signals on T lymphocyte development was investigated in transgenic mice expressing a dominant negative mutant protein, FADD-DN. Unexpectedly, FADD-DN enhanced negative selection of self-reactive thymic lymphocytes and inhibited T cell activation by increasing apoptosis. Thus signalling through FADD/MORT1 does not lead exclusively to cell death, but under certain circumstances can promote cell survival and proliferation.
摘要
含有死亡结构域的肿瘤坏死因子受体家族成员具有多效性活性。它们通过与细胞内FADD/MORT1相互作用诱导细胞凋亡，并通过TRADD和TRAF分子触发细胞生长或分化。在表达显性负性突变蛋白FADD-DN的转基因小鼠中，研究了FADD/MORT1转导信号对T淋巴细胞发育的影响。出乎意料的是，FADD-DN增强了自身反应性胸腺淋巴细胞的阴性选择，并通过增加细胞凋亡来抑制T细胞活化。因此，通过FADD/MORT1的信号传导并非仅导致细胞死亡，而是在某些情况下可促进细胞存活和增殖。
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