Dual Leucine Zipper Kinase Is Required for Retrograde Injury Signaling and Axonal Regeneration
- Authors
- Yongcheol Cho; Jung Eun Shin
- Issue Date
- 6월-2012
- Publisher
- CELL PRESS
- Citation
- NEURON, v.74, no.6, pp.1015 - 1022
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEURON
- Volume
- 74
- Number
- 6
- Start Page
- 1015
- End Page
- 1022
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/84541
- DOI
- 10.1016/j.neuron.2012.04.028
- ISSN
- 0896-6273
- Abstract
- Here we demonstrate that the dual leucine zipper kinase (DLK) promotes robust regeneration of peripheral axons after nerve injury in mice. Peripheral axon regeneration is accelerated by prior injury; however, DLK KO neurons do not respond to a preconditioning lesion with enhanced regeneration in vivo or in vitro. Assays for activation of transcription factors in injury-induced proregenerative pathways reveal that loss of DLK abolishes upregulation of p-STAT3 and p-cJun in the cell body after axonal injury. DLK is not required for the phosphorylation of STAT3 at the site of nerve injury but is necessary for retrograde transport of p-STAT3 to the cell body. These data demonstrate that DLK enhances regeneration by promoting a retrograde injury signal that is required for the activation of the neuronal proregenerative program.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.