A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration
Copyright policy )A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration
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.
- Washington University in St. Louis United States
- University of Mary United States
- Hope Center for Neurological Disorders United States
Anthracenes, Neurons, Green Fluorescent Proteins, JNK Mitogen-Activated Protein Kinases, Axotomy, Nerve Tissue Proteins, Embryo, Mammalian, MAP Kinase Kinase Kinases, Sciatic Nerve, Axons, Olfactory Receptor Neurons, Animals, Genetically Modified, Mice, Inbred C57BL, Disease Models, Animal, Mice, Ganglia, Spinal, Animals, Drosophila, Enzyme Inhibitors, Cells, Cultured
Anthracenes, Neurons, Green Fluorescent Proteins, JNK Mitogen-Activated Protein Kinases, Axotomy, Nerve Tissue Proteins, Embryo, Mammalian, MAP Kinase Kinase Kinases, Sciatic Nerve, Axons, Olfactory Receptor Neurons, Animals, Genetically Modified, Mice, Inbred C57BL, Disease Models, Animal, Mice, Ganglia, Spinal, Animals, Drosophila, Enzyme Inhibitors, Cells, Cultured
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