A mechanism of cell survival: Sequestration of Fas by the HGF receptor Met
A mechanism of cell survival: Sequestration of Fas by the HGF receptor Met
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DOI：
10.1016/s1097-2765(02)00439-2
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发表时间：
2002-02-01
期刊：
影响因子：
16
通讯作者：
Zarneger, R
中科院分区：
文献类型：
--
作者：
Wang, X;DeFrances, MC;Zarneger, R
Fas 等死亡受体存在于包括肝脏在内的多种器官中，在体内平衡中发挥重要作用。是什么阻止这些有害受体形成同源寡聚物、聚集和启动细胞凋亡途径尚不清楚。在这里，我们报告了一种细胞生存机制的发现，通过该机制 Met（一种生长因子受体酪氨酸激酶）直接结合并隔离肝细胞中的死亡受体 Fas。这种相互作用阻止Fas自聚集和Fas配体结合，从而抑制Fas激活和细胞凋亡。我们的结果描述了生长因子酪氨酸激酶受体和死亡受体之间的直接联系，以建立生长调节的新范例。
Death receptors such as Fas are present in a variety of organs including liver and play an important role in homeostasis. What prevents these harmful receptors from forming homooligomers, clustering, and initiating the apoptotic pathway is not known. Here, we report the discovery of a cell survival mechanism by which Met, a growth factor receptor tyrosine kinase, directly binds to and sequesters the death receptor Fas in hepatocytes. This interaction prevents Fas self-aggregation and Fas ligand binding, thus inhibiting Fas activation and apoptosis. Our results describe a direct link between growth factor tyrosine kinase receptors and death receptors to establish a novel paradigm in growth regulation.