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Title: Functional studies of BCLIIA : characterization of the conserved BCLIIA-XL splice variant and its interaction with BCL6 in nuclear paraspeckles of germinal center B cells
Authors: Liu, H.
Ippolito, G. C.
Wall, J. K.
Niu, T.
Probst, L.
Lee, B.-S.
Pulford, K.
Banham, A. H.
Stockwin, Luke
Shaffer, A. L.
Staudt, L. M.
Das, C.
Dyer, Martin J. S.
Tucker, P. W.
First Published: 16-May-2006
Publisher: BioMed Central
Citation: Molecular Cancer, 2006, 5 : 18
Abstract: Background: Chromosomal aberrations of BCL11A at 2p16.1 have been reported in a variety of B-cell malignancies and its deficiency in mice leads to a profound block in B-cell development. Results: Alternative pre-mRNA splicing of BCL11A produces multiple isoforms sharing a common N-terminus. The most abundant isoform we have identified in human lymphoid samples is BCL11A-XL, the longest transcript produced at this locus, and here we report the conservation of this major isoform and its functional characterization. We show that BCL11A-XL is a DNA-sequence-specific transcriptional repressor that associates with itself and with other BCL11A isoforms, as well as with the BCL6 proto-oncogene. Western blot data for BCL11A-XL expression coupled with data previously published for BCL6 indicates that these genes are expressed abundantly in germinal-center-derived B cells but that expression is extinguished upon terminal differentiation to the plasma cell stage. Although BCL11A-XL/BCL6 interaction can modulate BCL6 DNA binding in vitro, their heteromeric association does not alter the homomeric transcriptional properties of either on model reporter activity. BCL11A-XL partitions into the nuclear matrix and colocalizes with BCL6 in nuclear paraspeckles. Conclusion: We propose that the conserved N-terminus of BCL11A defines a superfamily of C2HC zinc-finger transcription factors involved in hematopoietic malignancies.
DOI Link: 10.1186/1476-4598-5-18
ISSN: 1476-4598
eISSN: 1476-4598
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2006 Liu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Appears in Collections:Published Articles, Dept. of Cancer Studies and Molecular Medicine

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