Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/24579
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
Links: http://hdl.handle.net/2381/24579
http://www.molecular-cancer.com/content/5/1/18
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 (http://creativecommons.org/licenses/by/2.0), 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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