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J. Biol. Chem., Vol. 281, Issue 22, 15505-15516, June 2, 2006

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Interaction of the B Cell-specific Transcriptional Coactivator OCA-B and Galectin-1 and a Possible Role in Regulating BCR-mediated B Cell Proliferation^*

From the Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, New York 10021

OCA-B is a B cell-specific transcriptional coactivator for OCT factors during the activation of immunoglobulin genes. In addition, OCA-B is crucial for B cell activation and germinal center formation. However, the molecular mechanisms for OCA-B function in these processes are not clear. Our previous studies documented two OCA-B isoforms and suggested a novel mechanism for the function of the myristoylated, membrane-bound form of OCA-B/p35 as a signaling molecule. Here, we report the identification of galectin-1, and related galectins, as a novel OCA-B-interacting protein. The interaction of OCA-B and galectin-1 can be detected both in vivo and in vitro. The galectin-1 binding domain in OCA-B has been localized to the N terminus of OCA-B. In B cells lacking OCA-B expression, increased galectin-1 expression, secretion, and cell surface association are observed. Consistent with these observations, and a reported inhibitory interaction of galectin-1 with CD45, the phosphatase activity of CD45 is reduced modestly, but significantly, in OCA-B-deficient B cells. Finally, galectin-1 is shown to negatively regulate B cell proliferation and tyrosine phosphorylation upon BCR stimulation. Together, these results raise the possibility that OCA-B may regulate BCR signaling through an association with galectin-1.

Received for publication, August 16, 2005 , and in revised form, March 23, 2006.

^* This work was supported in part by The Rockefeller University and National Institutes of Health Grant CA 113872 (to R. G. R.). 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1–S3.

¹ Supported by National Research Service Award Training Grant CA 09673-28A1 and fellowships from the Cancer Research Institute and Lymphoma Research Foundation.

² To whom correspondence should be addressed: 1230 York Ave., New York, NY 10021. Tel.: 212-327-7600; Fax: 212-327-7949; E-mail: roeder{at}mail.rockefeller.edu.

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