Proteasome inhibition induces neurite outgrowth through posttranslational modification of TrkA receptor
- Proteasome inhibition induces neurite outgrowth through posttranslational modification of TrkA receptor
- 송은주; 홍혜민; 유영숙
- Neurite Outgrowth; Proteasome inhibitor; TrkA receptor; MG132; Ubiquitination
- Issue Date
- The international journal of biochemistry & cell biology
- VOL 41, NO 3, 539-545
- The ubiquitin–proteasome pathway regulates many biological processes, including protein degradation, receptor endocytosis, protein sorting, subnuclear trafficking and neuronal differentiation. While proteasome inhibition is known to induce neurite outgrowth, the signaling mechanisms that mediate these effects have not been defined. In this study, we investigated the underlying mechanisms that link proteasome inhibition with neurite generation.We found that the proteasome inhibitors,MG132 and lactacystin, induced neurite outgrowthand also activated extracellular signal-regulated kinase/mitogen activated protein kinase and phosphatidylinositol-3-kinase/AKT pathways. These proteasome inhibitors also induced phosphorylation and ubiquitination of TrkA receptors, indicating that proteasome inhibition activates the major pathways of TrkA signaling. However, in contrast to nerve growth factor stimulation, which induces internalization of surface TrkA receptors, proteasome inhibitor-induced neurite outgrowth did not require TrkA receptor internalization. These results indicate that the ubiquitin–proteasome system regulates neurite formation through posttranslational modification of TrkA receptors.
- Appears in Collections:
- KIST Publication > Article
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.