JNK regulates FoxO-dependent autophagy in neurons

被引：181

作者：

Xu, Ping

Das, Madhumita

Reilly, Judith

Davis, Roger J. ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA

[2] Howard Hughes Med Inst, Worcester, MA 01605 USA

来源：

GENES & DEVELOPMENT | 2011年 / 25卷 / 04期

基金：

美国国家卫生研究院;

关键词：

autophagy; beclin; 1; Bnip3; JNK; neurons; N-TERMINAL KINASE; SIGNAL-TRANSDUCTION PATHWAY; FAST AXONAL-TRANSPORT; C-JUN; CEREBRAL-ISCHEMIA; TRANSCRIPTION FACTORS; CELL-DEATH; POSTMITOTIC NEURONS; PEPTIDE INHIBITOR; BRAIN-DEVELOPMENT;

D O I：

10.1101/gad.1984311

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

收藏

页码：310 / 322

页数：13

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