A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration.
Publication/Presentation Date
4-1-2009
Abstract
Axon degeneration underlies many common neurological disorders, but the signaling pathways that orchestrate axon degeneration are unknown. We found that dual leucine kinase (DLK) [corrected to add (DLK) abbreviation] promoted degeneration of severed axons in Drosophila and mice, and that its target, c-Jun N-terminal kinase, promoted degeneration locally in axons as they committed to degenerate. This pathway also promoted degeneration after chemotherapy exposure and may be a component of a general axon self-destruction program.
Volume
12
Issue
4
First Page
387
Last Page
389
ISSN
1546-1726
Published In/Presented At
Miller, B. R., Press, C., Daniels, R. W., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2009). A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration. Nature neuroscience, 12(4), 387–389. https://doi.org/10.1038/nn.2290
Disciplines
Medicine and Health Sciences | Pediatrics
PubMedID
19287387
Department(s)
Department of Pediatrics
Document Type
Article