| First Author | Khaled AR | Year | 2002 |
| Journal | Immunity | Volume | 17 |
| Issue | 5 | Pages | 561-73 |
| PubMed ID | 12433363 | Mgi Jnum | J:93139 |
| Mgi Id | MGI:3056018 | Doi | 10.1016/s1074-7613(02)00450-8 |
| Citation | Khaled AR, et al. (2002) Bax deficiency partially corrects interleukin-7 receptor alpha deficiency. Immunity 17(5):561-73 |
| abstractText | The requirement for cytokines in hematopoiesis is partly attributable to the protection of cells from apoptosis. Since IL-7 is required for normal T cell development, we evaluated the role of Bax in vivo by generating mice deficient in both Bax and the IL-7 receptor alpha chain (IL-7R). Starting at birth, we observed complete recovery of all stages of alphabeta thymocyte development up to 4 weeks of age. However, by 12 weeks of age, thymic cellularity had reverted to that of mice deficient in IL-7R alone. The BH3 only proteins, Bad and Bim, were also part of the death pathway repressed by IL-7. Thus, in young mice, Bax emerges as an essential protein in the death pathway induced by IL-7 deficiency. |
