JNK regulates FoxO-dependent autophagy in neurons
JNK regulates FoxO-dependent autophagy in neurons
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DOI：
10.1101/gad.1984311
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发表时间：
2011-02-15
影响因子：
10.5
通讯作者：
Davis, Roger J.
中科院分区：
文献类型：
--
作者：
Xu, Ping;Das, Madhumita;Davis, Roger J.
cJun N-末端激酶（JNK）信号转导通路涉及神经元功能的调节。JNK由三个基因编码，这些基因发挥部分冗余作用。在这里，我们报告了在神经元中靶向消融所有三个Jnk基因的小鼠的创建。化合物JNK缺陷神经元依赖于自噬存活。这种自噬反应是由FoxO诱导的Bnip 3表达引起的，Bnip 3从失活的Bcl-XL复合物中置换自噬效应子Beclin-1。这些数据将JNK鉴定为神经元中FoxO依赖性自噬的有效负调节剂。
The cJun N-terminal kinase (JNK) signal transduction pathway is implicated in the regulation of neuronal function. JNK is encoded by three genes that play partially redundant roles. Here we report the creation of mice with targeted ablation of all three Jnk genes in neurons. Compound JNK-deficient neurons are dependent on autophagy for survival. This autophagic response is caused by FoxO-induced expression of Bnip3 that displaces the autophagic effector Beclin-1 from inactive Bcl-XL complexes. These data identify JNK as a potent negative regulator of FoxO-dependent autophagy in neurons.