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J. Biol. Chem., Vol. 283, Issue 36, 24326-24333, September 5, 2008

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GABPβ2 Is Dispensible for Normal Lymphocyte Development but Moderately Affects B Cell Responses^*

Xuefang Jing, Dong-Mei Zhao, Thomas J. Waldschmidt, and Hai-Hui Xue¹

From the Departments of Microbiology and Pathology, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242

GA-binding protein (GABP) is the only Ets family transcription factor that functions as a heterodimer. The GABP subunit binds to DNA, and the GABPβ subunit possesses the ability to transactivate target genes. Inactivation of GABP caused embryonic lethality and defective lymphocyte development and immune responses. There are 3 isoforms of the GABPβ subunit, but whether they have distinct functions has not been addressed. In this study, we selectively ablated the expression of GABPβ2 using a gene trap strategy. GABPβ2-deficient mice were viable and had normal T and B cell development, suggesting that loss of GABPβ2 is compensated for by other GABPβ isoforms during these processes. GABPβ2-deficient T cells can be activated and proliferate similarly to wild-type controls. In contrast, B cells lacking GABPβ2 showed 2–3-fold increases in proliferation in response to B cell receptor stimulation. In addition, GABPβ2-deficient mice exhibited moderately increased antibody production and germinal center responses when challenged with T-dependent antigens. These results indicate that albeit GABPβ isoforms are redundant in lymphocyte development, GABPβ2 has a distinct role in restraining B cell expansion and humoral responses.

Received for publication, June 12, 2008 , and in revised form, July 7, 2008.

^* 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.

¹ To whom correspondence should be addressed: 51 Newton Rd. BSB 3–710, IA City, IA 52246. Tel.: 319-335-7937; Fax: 319-335-9006; E-mail: hai-hui-xue{at}uiowa.edu.

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