期刊
GENES & DEVELOPMENT
卷 25, 期 4, 页码 310-322出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1984311
关键词
autophagy; beclin 1; Bnip3; JNK; neurons
资金
- National Institutes of Health [NS054948]
- NIDDK Diabetes and Endocrinology Research Center [DK32520]
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.
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