| First Author | Zou Q | Year | 2015 |
| Journal | J Exp Med | Volume | 212 |
| Issue | 8 | Pages | 1323-36 |
| PubMed ID | 26195727 | Mgi Jnum | J:226431 |
| Mgi Id | MGI:5697254 | Doi | 10.1084/jem.20150110 |
| Citation | Zou Q, et al. (2015) T cell development involves TRAF3IP3-mediated ERK signaling in the Golgi. J Exp Med 212(8):1323-36 |
| abstractText | Generation of T lymphocytes in the thymus is guided by signal transduction from the T cell receptor (TCR), but the underlying mechanism is incompletely understood. Here we have identified a Golgi-associated factor, TRAF3-interacting protein 3 (TRAF3IP3), as a crucial mediator of thymocyte development. TRAF3IP3 deficiency in mice attenuates the generation of mature thymocytes caused by impaired thymocyte-positive selection. TRAF3IP3 mediates TCR-stimulated activation of the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) and its upstream kinase mitogen/extracellular signal-regulated kinase (MEK). Interestingly, TRAF3IP3 exerts this signaling function through recruiting MEK to the Golgi and, thereby, facilitating the interaction of MEK with its activator BRAF. Transgenic expression of a constitutively active MEK rescues the T cell development block in Traf3ip3 knockout mice. These findings establish TRAF3IP3 as a novel regulator of T cell development and suggest a Golgi-specific ERK signaling mechanism that regulates thymocyte development. |
