| First Author | Rho J | Year | 2001 |
| Journal | Mol Cell Biol | Volume | 21 |
| Issue | 24 | Pages | 8365-70 |
| PubMed ID | 11713273 | Mgi Jnum | J:72947 |
| Mgi Id | MGI:2154031 | Doi | 10.1128/MCB.21.24.8365-8370.2001 |
| Citation | Rho J, et al. (2001) TDAG51 Is Not Essential for Fas/CD95 Regulation and Apoptosis In Vivo. Mol Cell Biol 21(24):8365-70 |
| abstractText | Fas/CD95 is a key regulator of apoptotic signaling, which is crucial for the maintenance of homeostasis in peripheral lymphoid organs. TDAG51 has been shown to play critical roles in the up-regulation of Fas gene expression and T-cell apoptosis in vitro. In order to identify the role of TDAG51 in vivo, we generated TDAG51-deficient (TDAG51(-/-)) mice. Northern blotting revealed no expression of TDAG51 in TDAG51(-/-) mice, indicating that the TDAG51 gene was successfully targeted. TDAG51(-/-) mice were healthy and showed no gross developmental abnormalities. While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51(-/-) mice had no apparent defects in secondary lymphoid organs. Although TDAG51 is required for up-regulation of Fas expression in T-cell hybridomas, TDAG51(-/-) mice expressed normal levels of Fas and had normal T-cell apoptosis. Therefore, we conclude that TDAG51 is not essential for Fas up-regulation and T-cell apoptosis in vivo. There are several known homologs of TDAG51, and these homologs may substitute for TDAG51 in TDAG51(-/-) mice. |
