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Blood, 15 September 2005, Vol. 106, No. 6, pp. 2105-2112. Prepublished online as a Blood First Edition Paper on May 5, 2005; DOI 10.1182/blood-2004-04-1248. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-04-1248v1 106/6/2105    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Tian, M. T. Articles by DeFranco, A. L. Search for Related Content PubMed PubMed Citation Articles by Tian, M. T. Articles by DeFranco, A. L. Related Collections Apoptosis Immunobiology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Bcl10 can promote survival of antigen-stimulated B lymphocytes Maoxin Tim Tian, Gabriel Gonzalez, Barbara Scheer, and Anthony L. DeFranco From the G.W. Hooper Foundation, San Francisco, CA; and the Department of Microbiology and Immunology, University of California, San Francisco, CA. To understand the nature of negative responses through the B-cell antigen receptor (BCR), we have screened an expression cDNA library for the ability to block BCR-induced growth arrest and apoptosis in the immature B-cell line, WEHI-231. We isolated multiple copies of full-length, unmutated Bcl10, a signaling adaptor molecule encoded by a gene found to translocate to the immunoglobulin heavy chain (IgH) locus in some mucosa-associated lymphoid tissue (MALT) lymphomas. A conditionally active form of B-cell lymphoma 10 (Bcl10) protected WEHI-231 cells from BCR-induced apoptosis upon activation. Induction of Bcl10 activity caused rapid activation of nuclear factor-B (NF-B) and c-Jun N-terminal kinase (JNK), but not activation of extracellular signal-regulated kinase (ERK) or p38 mitogen-activated protein (MAP) kinases. These results support genetic and biochemical experiments that have implicated Bcl10 and its binding partners Carma1 and MALT1 in mediating the ability of the BCR to activate NF-B. The ability of Bcl10 expression to prevent BCR-induced growth arrest and apoptosis of WEHI-231 cells was dependent on NF-B activation. Finally, overexpression of Bcl10 in primary B cells activated ex vivo promoted the survival of these cells after removal of activating stimuli. Taken together these results support the hypothesis that enhanced BCL10 expression caused by translocation to the IGH locus can promote formation of MALT lymphomas. (Blood. 2005;106:2105-2112) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Bhattacharyya, A. Borthakur, N. Pant, P. K. Dudeja, and J. K. Tobacman Bcl10 mediates LPS-induced activation of NF-{kappa}B and IL-8 in human intestinal epithelial cells Am J Physiol Gastrointest Liver Physiol, August 1, 2007; 293(2): G429 - G437. [Abstract] [Full Text] [PDF] M-Q Du and J C Atherton Molecular subtyping of gastric MALT lymphomas: implications for prognosis and management. Gut, June 1, 2006; 55(6): 886 - 893. [Full Text] [PDF]

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