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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2495-2503. Prepublished online as a Blood First Edition Paper on November 23, 2004; DOI 10.1182/blood-2004-09-3644. This Article Full Text (PDF) All Versions of this Article: 2004-09-3644v1 105/6/2495    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 Oppezzo, P. Articles by Vuillier, F. Search for Related Content PubMed PubMed Citation Articles by Oppezzo, P. Articles by Vuillier, F. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 21, 2004 Accepted November 17, 2004 Different isoforms of BSAP regulate expression of AID in normal and chronic lymphocytic leukemia B-cells Pablo Oppezzo*, Gerard Dumas, Ana I Lalanne, Beatrice Payelle-Brogard, Christian Magnac, Otto Pritsch, Guillaume Dighiero, and Francoise Vuillier Unite d'Immuno-hematologie et d'Immunopathologie, Institut Pasteur, Paris, France Departamento de Bioquimica, Facultad de Medicina de Montevideo, Montevideo, Uruguay * Corresponding author; email: poppezzo{at}pasteur.fr. Activation induced cytidine deaminase (AID) is key to initiating somatic hypermutation (SHM) and class switch recombination (CSR), but its mode of action and regulation remains unclear. Since, Pax-5 and Id-2 transcription factors plays an opposed role in AID regulation, we have studied the expression of Pax-5, Id-2 and prdm-1 genes, in 54 chronic lymphocytic leukaemia (CLL) B-cells. Our results show that: 1) in 21 cases, presence of AID is constantly associated with high expression of the complete form of Pax-5 gene (Pax-5a) and lower expression of Id-2 and prdm-1 transcripts. 2) in 33 cases, the absence of AID expression and CSR is associated to a reduction of Pax-5a and the appearance of a spliced form with a deletion in exon 8 (Pax-5/-Ex8). 3) stimulation with CD40L+IL4 induces CSR, presence of AID transcripts, up-regulation of Pax-5a and down-regulation of Pax-5/-Ex8, Id-2 and prdm-1 transcripts. 4) Pax-5a and Pax-5/-Ex8 are translated into two isoforms of the B-cell specific activator protein (BSAP) and are both able to bind the AID-promoter region. Overall, these results suggest that Pax-5/-Ex8, could play an important role in the control of its own transcription and indirectly in AID expression and CSR. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Nagaoka, T. H. Tran, M. Kobayashi, M. Aida, and T. Honjo Preventing AID, a physiological mutator, from deleterious activation: regulation of the genomic instability that is associated with antibody diversity Int. Immunol., March 5, 2010; (2010) dxq023v1. [Abstract] [Full Text] [PDF] G. A. Robichaud, J.-P. Perreault, and R. J. Ouellette Development of an isoform-specific gene suppression system: the study of the human Pax-5B transcriptional element Nucleic Acids Res., August 1, 2008; 36(14): 4609 - 4620. [Abstract] [Full Text] [PDF]

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