BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes
(2006) In Blood 108(8). p.2695-2702- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1137544
- author
- Cismasiu, Valeriu LU ; Ghanta, Sailaja ; Duque, Javier ; Albu, Diana I ; Chen, Hong-Mei ; Kasturi, Rohini and Avram, Dorina
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 108
- issue
- 8
- pages
- 2695 - 2702
- publisher
- American Society of Hematology
- external identifiers
-
- pmid:16809611
- scopus:33750607751
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2006-05-021790
- language
- English
- LU publication?
- yes
- id
- 5d95af2b-70a4-4f5c-996b-657d16d8afbc (old id 1137544)
- date added to LUP
- 2016-04-01 12:28:44
- date last changed
- 2022-06-09 18:59:18
@article{5d95af2b-70a4-4f5c-996b-657d16d8afbc, abstract = {{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.}}, author = {{Cismasiu, Valeriu and Ghanta, Sailaja and Duque, Javier and Albu, Diana I and Chen, Hong-Mei and Kasturi, Rohini and Avram, Dorina}}, issn = {{1528-0020}}, language = {{eng}}, number = {{8}}, pages = {{2695--2702}}, publisher = {{American Society of Hematology}}, series = {{Blood}}, title = {{BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes}}, url = {{http://dx.doi.org/10.1182/blood-2006-05-021790}}, doi = {{10.1182/blood-2006-05-021790}}, volume = {{108}}, year = {{2006}}, }