| First Author | Cismasiu VB | Year | 2006 |
| Journal | Blood | Volume | 108 |
| Issue | 8 | Pages | 2695-702 |
| PubMed ID | 16809611 | Mgi Jnum | J:139460 |
| Mgi Id | MGI:3808092 | Doi | 10.1182/blood-2006-05-021790 |
| Citation | Cismasiu VB, et al. (2006) BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes. Blood 108(8):2695-702 |
| abstractText | BCL11A and BCL11B are transcriptional regulators important for lymphopoiesis and previously associated with hematopoietic malignancies. Ablation of the mouse Bcl11b locus results in failure to generate double-positive thymocytes, implicating a critical role of Bcl11b in T-cell development. However, BCL11B is also expressed in CD4+ T lymphocytes, both in resting and activated states. Here we show both in transformed and primary CD4+ T cells that BCL11B participates in the control of the interleukin-2 (IL2) gene expression following activation through T-cell receptor (TCR). BCL11B augments expression from the IL2 promoter through direct binding to the US1 site. In addition, BCL11B associates with the p300 coactivator in CD4+ T cells activated through TCR, which may account for its transcriptional activation function. These results provide the first evidence that BCL11B, originally described as a transcriptional repressor, activates transcription of a target gene in the context of T-cell activation. |
