| First Author | Shin JE | Year | 2019 |
| Journal | Neurobiol Dis | Volume | 127 |
| Pages | 178-192 | PubMed ID | 30735704 |
| Mgi Jnum | J:283596 | Mgi Id | MGI:6355714 |
| Doi | 10.1016/j.nbd.2019.02.001 | Citation | Shin JE, et al. (2019) DLK regulates a distinctive transcriptional regeneration program after peripheral nerve injury. Neurobiol Dis 127:178-192 |
| abstractText | Following damage to a peripheral nerve, injury signaling pathways converge in the cell body to generate transcriptional changes that support axon regeneration. Here, we demonstrate that dual leucine zipper kinase (DLK), a central regulator of injury responses including axon regeneration and neuronal apoptosis, is required for the induction of the pro-regenerative transcriptional program in response to peripheral nerve injury. Using a sensory neuron-conditional DLK knockout mouse model, we show a time course for the dependency of gene expression changes on the DLK pathway after sciatic nerve injury. Gene ontology analysis reveals that DLK-dependent gene sets are enriched for specific functional annotations such as ion transport and immune response. A series of comparative analyses shows that the DLK-dependent transcriptional program is distinct from that promoted by the importin-dependent retrograde signaling pathway, while it is partially shared between PNS and CNS injury responses. We suggest that DLK-dependency might provide a selective filter for regeneration-associated genes among the injury-responsive transcriptome. |
