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Nat Neurosci. 2009 Apr;12(4):387-9. doi: 10.1038/nn.2290. Epub 2009 Mar 15.

A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration.

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1
Department of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.

Erratum in

  • Nat Neurosci. 2009 Jun;12(6):808.

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.

PMID:
19287387
PMCID:
PMC2696160
DOI:
10.1038/nn.2290
[Indexed for MEDLINE]
Free PMC Article

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