| First Author | Belin S | Year | 2015 |
| Journal | Neuron | Volume | 86 |
| Issue | 4 | Pages | 1000-1014 |
| PubMed ID | 25937169 | Mgi Jnum | J:255119 |
| Mgi Id | MGI:6109623 | Doi | 10.1016/j.neuron.2015.03.060 |
| Citation | Belin S, et al. (2015) Injury-induced decline of intrinsic regenerative ability revealed by quantitative proteomics. Neuron 86(4):1000-1014 |
| abstractText | Neurons differ in their responses to injury, but the underlying mechanisms remain poorly understood. Using quantitative proteomics, we characterized the injury-triggered response from purified intact and axotomized retinal ganglion cells (RGCs). Subsequent informatics analyses revealed a network of injury-response signaling hubs. In addition to confirming known players, such as mTOR, this also identified new candidates, such as c-myc, NFkappaB, and Huntingtin. Similar to mTOR, c-myc has been implicated as a key regulator of anabolic metabolism and is downregulated by axotomy. Forced expression of c-myc in RGCs, either before or after injury, promotes dramatic RGC survival and axon regeneration after optic nerve injury. Finally, in contrast to RGCs, neither c-myc nor mTOR was downregulated in injured peripheral sensory neurons. Our studies suggest that c-myc and other injury-responsive pathways are critical to the intrinsic regenerative mechanisms and might represent a novel target for developing neural repair strategies in adults. |
