Ligation of B cell receptor (BCR) on BKS-2, an immature B cell lymphoma by anti-IgM antibodies (Ab) caused apoptosis. Here we report that signaling through B cell receptor in wild type BKS-2 cells down-regulated the expression of Egr-1, a zinc finger-containing transcription factor. A reduction in the level ofEgr-1 mRNA could be demonstrated as early as 30 min after the ligation of BCR on BKS-2 cells. Immunocytochemical and Western blot analysis revealed that the expression of EGR-1 protein was also inhibited by anti-IgM treatment. Antisense oligonucleotides to Egr-1 caused growth inhibition and apoptosis in BKS-2 cells, suggesting that expression of Egr-1 is important for the survival of these B lymphoma cells. In contrast to wild type BKS-2 cells, the mutant 1.B5 cell line, which is refractory to B cell receptor-mediated growth-inhibitory signals, showed an increased expression of Egr-1 upon treatment with anti-IgM. These results implicate a role for Egr-1 in blocking B cell receptor-mediated apoptosis in immature B cells.

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Published in The Journal of Biological Chemistry, v. 272, no. 44, p. 27987-27993.

This research was originally published in The Journal of Biological Chemistry. Subramanian Muthukkumar, Seong-Su Han, Sumathi Muthukkumar, Vivek M. Rangnekar, and Subbarao Bondada. Role of Egr-1 Gene Expression in B Cell Receptor-induced Apoptosis in an Immature B Cell Lymphoma. J. Biol. Chem. 1997; 272:27987-27993. © 1997 by The American Society for Biochemistry and Molecular Biology, Inc.

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This work was supported in part by Grants AI 21490 and AG 05731 (to S. B.) from the National Institutes of Health. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.