Program in Molecular Medicine
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
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Developmental Biology | Developmental Neuroscience | Molecular and Cellular Neuroscience | Molecular Biology | Molecular Genetics
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.
autophagy, Beclin 1, Bnip3, JNK, Neurons
Rights and Permissions
Copyright © 2011 by Cold Spring Harbor Laboratory Press. Freely available online through the Genes and Development Open Access option.
DOI of Published Version
Genes Dev. 2011 Feb 15;25(4):310-22. doi: 10.1101/gad.1984311. Link to article on publisher's site
Genes and development
Xu P, Das M, Reilly J, Davis RJ. (2011). JNK regulates FoxO-dependent autophagy in neurons. Davis Lab Publications. https://doi.org/10.1101/gad.1984311. Retrieved from https://escholarship.umassmed.edu/davis/30
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