| First Author | Muro R | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 496 |
| Issue | 1 | Pages | 25-30 |
| PubMed ID | 29291408 | Mgi Jnum | J:271448 |
| Mgi Id | MGI:6280274 | Doi | 10.1016/j.bbrc.2017.12.159 |
| Citation | Muro R, et al. (2018) Rasal3-mediated T cell survival is essential for inflammatory responses. Biochem Biophys Res Commun 496(1):25-30 |
| abstractText | Fine regulation of the Ras/mitogen-activating protein kinase (MAPK) pathway is crucial in controlling the survival, proliferation, and development of various types of cells. Ras-activating protein-like 3 (Rasal3) is a T cell-specific Ras GTPase-activating protein that negatively regulates T cell receptor (TCR)-induced activation of Ras/MAPK pathway. Rasal3-deficient mice showed a decreased number of naive T cells because Rasal3 is required for the survival of naive T cells. In the current study, we observed ameliorated Type1 T helper (Th1) cell- and Type2 T helper (Th2) cell-dependent contact hypersensitivity reactions in Rasal3-deficient mice, along with a marked shortage of T cells at regional lymph node. Activated Rasal3-deficient T cells showed an increased cell death with reduced Bcl2 expression, suggesting that Rasal3 is required for the survival of not only naive T cells but also activated T cells. Collectively, Rasal3 controls the magnitude of inflammatory responses through the survival of both naive T cells and activated T cells in vivo. |
