RIP3, a novel apoptosis-inducing kinase
RIP3, a novel apoptosis-inducing kinase
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DOI：
10.1074/jbc.274.24.16871
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发表时间：
1999-06-11
影响因子：
4.8
通讯作者：
Dixit, VM
中科院分区：
文献类型：
--
作者：
Sun, XQ;Lee, J;Dixit, VM
RIPS是一种新的基因产物，其N-末端激酶结构域与RIP（受体相互作用蛋白）和RIPE中的相应结构域具有广泛的同源性。与具有C末端死亡结构域的RIP和具有C末端胱天蛋白酶激活和募集结构域的RIPE不同，RIPS具有独特的C末端。RIPS通过其独特的C-末端片段结合RIP，并且凭借这种相互作用被募集到肿瘤坏死因子（TNF）受体-1信号传导复合物。先前的研究表明RIP介导TNF诱导的抗凋亡NF-κ B通路的激活。然而，RIPS减弱RIP和TNF受体-1诱导的NF-κ B活化。过表达研究表明，RIPS是一种有效的诱导凋亡，能够选择性地结合到大的前结构域启动子半胱天冬酶。
RIPS is a novel gene product containing a N-terminal kinase domain that shares extensive homology with the corresponding domain in RIP (receptor-interacting protein) and RIPE. Unlike RIP, which has a C-terminal death domain, and RIPE, which has a C-terminal caspase activation and recruitment domain, RIPS has a unique C terminus. RIPS binds RIP through its unique C-terminal segment and by virtue of this interaction is recruited to the tumor necrosis factor (TNF) receptor-1 signaling complex. Previous studies have shown that RIP mediates TNF-induced activation of the anti-apoptotic NF-KB pathway. RIPS, however, attenuates both RIP and TNF receptor-1-induced NF-KB activation. Overexpression studies revealed RIPS to be a potent inducer of apoptosis, capable of selectively binding to large prodomain initiator caspases.