| Literature DB >> 21325132 |
Ping Xu1, Madhumita Das, Judith Reilly, Roger J Davis.
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.Entities:
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Year: 2011 PMID: 21325132 PMCID: PMC3042155 DOI: 10.1101/gad.1984311
Source DB: PubMed Journal: Genes Dev ISSN: 0890-9369 Impact factor: 11.361