| First Author | Levin SD | Year | 1993 |
| Journal | EMBO J | Volume | 12 |
| Issue | 4 | Pages | 1671-80 |
| PubMed ID | 8385609 | Mgi Jnum | J:76887 |
| Mgi Id | MGI:2180494 | Doi | 10.1002/j.1460-2075.1993.tb05812.x |
| Citation | Levin SD, et al. (1993) A dominant-negative transgene defines a role for p56lck in thymopoiesis. EMBO J 12(4):1671-80 |
| abstractText | The lymphocyte-specific protein tyrosine kinase p56lck participates in T cell signaling through functional interactions with components of the T cell antigen receptor complex and the interleukin-2 receptor. Additional insight into the function of p56lck has now been obtained through the generation of transgenic animals expressing high levels of a catalytically inactive form of this kinase (p56lckR273). Mice bearing the lckR273 transgene manifested a severe defect in the production of virtually all T lymphocytes. Those exceptional CD3+ cells that escaped the effects of the lckR273 transgene were confined primarily to the T cell subset that expresses gamma/delta T cell receptors. Remarkably, construction of a dose-response curve for the effects of the lckR273 transgene revealed that developmental arrest of thymocytes occurred at a discrete stage in the normal T cell maturation pathway, corresponding to a point at which thymoblasts ordinarily begin a series of mitotic divisions that result in expansion and maturation. These results suggest that p56lck normally regulates T cell production by metering the replicative potential of immature thymoblasts. |
