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BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes

Cismasiu, Valeriu LU ; Ghanta, Sailaja ; Duque, Javier ; Albu, Diana I ; Chen, Hong-Mei ; Kasturi, Rohini and Avram, Dorina (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)
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author
; ; ; ; ; and
organization
publishing date
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}},
}