JNK regulates the release of proapoptotic mitochondrial factors in reovirus-infected cells
JNK regulates the release of proapoptotic mitochondrial factors in reovirus-infected cells
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DOI：
10.1128/jvi.78.23.13132-13138.2004
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发表时间：
2004-12-01
影响因子：
5.4
通讯作者：
Tyler, KL
中科院分区：
文献类型：
--
作者：
Clarke, P;Meintzer, SM;Tyler, KL
呼肠孤病毒诱导的细胞凋亡与促凋亡的丝裂原活化蛋白激酶c-jun氨基末端激酶(JNK)和JNK相关的转录因子c-jun有关。在这里，我们发现呼肠孤病毒诱导的细胞凋亡和caspase 3的激活在缺乏呼肠孤病毒感染细胞中JNK的上游激活物MEK激酶1的细胞中受到抑制。在呼肠孤病毒感染后抑制JNK活性会延迟促凋亡线粒体因子的释放和随后的细胞凋亡的发生。反之，携带显性阴性c-jun的腺病毒感染不能阻断呼肠孤病毒诱导的细胞凋亡，并且c-jun的激活与呼肠孤病毒感染细胞中的细胞凋亡无关。这是第一个证明JNK与病毒感染后线粒体凋亡途径的调节有关的报告。
Reovirus-induced apoptosis is associated with activation of the proapoptotic mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) and the JNK-associated transcription factor c-Jun. Here we show that reovirus-induced apoptosis and activation of caspase 3 are inhibited in cells deficient in MEK kinase 1, an upstream activator of JNK in reovirus-infected cells. Inhibition of JNK activity following reovirus infection delays the release of proapoptotic mitochondrial factors and the subsequent onset of apoptosis. In contrast, reovirus-induced apoptosis is not blocked by infection with adenovirus expressing dominant-negative c-Jun, and c-Jun activation does not correlate with apoptosis in reovirus-infected cells. This is the first report demonstrating that JNK is associated with regulation of mitochondrial pathways of apoptosis following viral infection.