| First Author | Storck S | Year | 2005 |
| Journal | Mol Cell Biol | Volume | 25 |
| Issue | 4 | Pages | 1437-45 |
| PubMed ID | 15684394 | Mgi Jnum | J:95986 |
| Mgi Id | MGI:3528525 | Doi | 10.1128/MCB.25.4.1437-1445.2005 |
| Citation | Storck S, et al. (2005) Normal immune system development in mice lacking the Deltex-1 RING finger domain. Mol Cell Biol 25(4):1437-45 |
| abstractText | The Notch signaling pathway controls several cell fate decisions during lymphocyte development, from T-cell lineage commitment to the peripheral differentiation of B and T lymphocytes. Deltex-1 is a RING finger ubiquitin ligase which is conserved from Drosophila to humans and has been proposed to be a regulator of Notch signaling. Its pattern of lymphoid expression as well as gain-of-function experiments suggest that Deltex-1 regulates both B-cell lineage and splenic marginal-zone B-cell commitment. Deltex-1 was also found to be highly expressed in germinal-center B cells. To investigate the physiological function of Deltex-1, we generated a mouse strain lacking the Deltex-1 RING finger domain, which is essential for its ubiquitin ligase activity. Deltex-1(Delta/Delta) mice were viable and fertile. A detailed histological analysis did not reveal any defects in major organs. T- and B-cell development was normal, as were humoral responses against T-dependent and T-independent antigens. These data indicate that the Deltex-1 ubiquitin ligase activity is dispensable for mouse development and immune function. Possible compensatory mechanisms, in particular those from a fourth Deltex gene identified during the course of this study, are also discussed. |
