UMMS Affiliation

Program in Molecular Medicine

Date

2-15-2011

Document Type

Article

Medical Subject Headings

Animals; Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Cells, Cultured; Forkhead Transcription Factors; JNK Mitogen-Activated Protein Kinases; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondrial Proteins; Neurons; Signal Transduction; Transcription Factors

Disciplines

Biochemistry | Cell Biology | Cellular and Molecular Physiology | Developmental Biology | Developmental Neuroscience | Molecular and Cellular Neuroscience | Molecular Biology | Molecular Genetics

Abstract

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.

Rights and Permissions

Citation: Genes Dev. 2011 Feb 15;25(4):310-22. doi: 10.1101/gad.1984311. Link to article on publisher's site

Comments

Copyright © 2011 by Cold Spring Harbor Laboratory Press. Freely available online through the Genes & Development Open Access option.

Related Resources

Link to Article in PubMed

Keywords

autophagy, Beclin 1, Bnip3, JNK, Neurons

PubMed ID

21325132

 
 

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