期刊
BLOOD
卷 108, 期 8, 页码 2695-2702出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-05-021790
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- NHLBI NIH HHS [T32 HL 07194] Funding Source: Medline
- NIAMS NIH HHS [K01 AR 02914] Funding Source: Medline
BCL11A and BCL11B are transcriptional regulators important for lymphopoiesis and previously associated with hematopoletic 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 BCL11 B participates in the control of the interleukin-2 (IL2) gene expression following activation through T-cell receptor (TCR). BCL11 B augments expression from the IL2promoter through direct binding to the US1 site. In addition, BCL11 B 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.
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