UMass Chan Affiliations
Program in Molecular MedicineDocument Type
Journal ArticlePublication Date
2011-02-15Keywords
AnimalsApoptosis
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
autophagy
Beclin 1
Bnip3
JNK
Neurons
Biochemistry
Cell Biology
Cellular and Molecular Physiology
Developmental Biology
Developmental Neuroscience
Molecular and Cellular Neuroscience
Molecular Biology
Molecular Genetics
Metadata
Show full item recordAbstract
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.Source
Genes Dev. 2011 Feb 15;25(4):310-22. doi: 10.1101/gad.1984311. Link to article on publisher's site
DOI
10.1101/gad.1984311Permanent Link to this Item
http://hdl.handle.net/20.500.14038/28301PubMed ID
21325132Related Resources
Rights
Copyright © 2011 by Cold Spring Harbor Laboratory Press. Freely available online through the Genes and Development Open Access option.ae974a485f413a2113503eed53cd6c53
10.1101/gad.1984311