Work

JNK regulates FoxO-dependent autophagy in neurons

Year: 2011

Type: preprint

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.

Source: Genes & Development

DOI: 10.1101/gad.1984311

Authors: Ping Xu, Madhumita Das, Judith Reilly, Roger J. Davis

Institutions: University of Massachusetts Chan Medical School, Howard Hughes Medical Institute

Language: English

Topic: Autophagy in Disease and Therapy

Subfield: Cell Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funders: Howard Hughes Medical Institute, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Neurological Disorders and Stroke