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Blood, 15 October 2006, Vol. 108, No. 8, pp. 2695-2702. Prepublished online as a Blood First Edition Paper on June 29, 2006; DOI 10.1182/blood-2006-05-021790. This Article Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-05-021790v1 108/8/2695    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cismasiu, V. B Articles by Avram, D. Search for Related Content PubMed PubMed Citation Articles by Cismasiu, V. B Articles by Avram, D. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 12, 2005 Accepted June 9, 2006 BCL11B participates in the activation of interleukin-2 gene expression in CD4+ T lymphocytes Valeriu B Cismasiu, Sailaja Ghanta, Javier Duque, Diana Albu, Hong-Mei Chen, Rohini Kasturi, and Dorina Avram* Center for Cell Biology and Cancer Research, Albany Medical College, Albany, NY, USA * Corresponding author; email: avramd{at}mail.amc.edu. 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 interleukin-2 (IL-2) gene expression following activation through T cell receptor (TCR). BCL11B augments expression from IL-2 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. M. Lauberth, A. C. Bilyeu, B. A. Firulli, K. L. Kroll, and M. Rauchman A Phosphomimetic Mutation in the Sall1 Repression Motif Disrupts Recruitment of the Nucleosome Remodeling and Deacetylase Complex and Repression of Gbx2 J. Biol. Chem., November 30, 2007; 282(48): 34858 - 34868. [Abstract] [Full Text] [PDF] D. I. Albu, D. Feng, D. Bhattacharya, N. A. Jenkins, N. G. Copeland, P. Liu, and D. Avram BCL11B is required for positive selection and survival of double-positive thymocytes J. Exp. Med., November 26, 2007; 204(12): 3003 - 3015. [Abstract] [Full Text] [PDF] C. C. Tydell, E.-S. David-Fung, J. E. Moore, L. Rowen, T. Taghon, and E. V. Rothenberg Molecular Dissection of Prethymic Progenitor Entry into the T Lymphocyte Developmental Pathway J. Immunol., July 1, 2007; 179(1): 421 - 438. [Abstract] [Full Text] [PDF] S. Nagel, M. Scherr, A. Kel, K. Hornischer, G. E. Crawford, M. Kaufmann, C. Meyer, H. G. Drexler, and R. A.F. MacLeod Activation of TLX3 and NKX2-5 in t(5;14)(q35;q32) T-Cell Acute Lymphoblastic Leukemia by Remote 3'-BCL11B Enhancers and Coregulation by PU.1 and HMGA1 Cancer Res., February 15, 2007; 67(4): 1461 - 1471. [Abstract] [Full Text] [PDF] X.-Y. Su, V. Della-Valle, I. Andre-Schmutz, C. Lemercier, I. Radford-Weiss, P. Ballerini, M. Lessard, M. Lafage-Pochitaloff, F. Mugneret, R. Berger, et al. HOX11L2/TLX3 is transcriptionally activated through T-cell regulatory elements downstream of BCL11B as a result of the t(5;14)(q35;q32) Blood, December 15, 2006; 108(13): 4198 - 4201. [Abstract] [Full Text] [PDF]

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