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

Xuefang Jing; Dong-Mei Zhao; Thomas J Waldschmidt; Hai-Hui Xue

doi:10.1074/jbc.M804487200

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

Journal article

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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 Xue

The Journal of biological chemistry, Vol.283(36), pp.24326-24333

09/05/2008

DOI: 10.1074/jbc.M804487200

PMCID: PMC3259847

PMID: 18628204

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Abstract

GA-binding protein (GABP) is the only Ets family transcription factor that functions as a heterodimer. The GABPα subunit binds to DNA, and the GABPβ subunit possesses the ability to transactivate target genes. Inactivation of GABPα 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.

Molecular Basis of Cell and Developmental Biology

Details

Title: Subtitle: GABPβ2 Is Dispensible for Normal Lymphocyte Development but Moderately Affects B Cell Responses
Creators: Xuefang Jing - Departments of
Dong-Mei Zhao - Departments of
Thomas J Waldschmidt - Departments of
Hai-Hui Xue - Departments of
Resource Type: Journal article
Publication Details: The Journal of biological chemistry, Vol.283(36), pp.24326-24333
DOI: 10.1074/jbc.M804487200
PMID: 18628204
PMCID: PMC3259847
NLM abbreviation: J Biol Chem
ISSN: 0021-9258
eISSN: 1083-351X
Publisher: American Society for Biochemistry and Molecular Biology
Language: English
Date published: 09/05/2008
Academic Unit: Microbiology and Immunology; Pathology
Record Identifier: 9984047775602771

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