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Molecular and Cellular Biology, January 2004, p. 719-729, Vol. 24, No. 2
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.2.719-729.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Immunological Function in Mice Lacking the Rac-Related GTPase RhoG

Elena Vigorito,^1* Sarah Bell,¹ Barbara J. Hebeis,¹ Helen Reynolds,¹ Simon McAdam,¹ Piers C. Emson,² Andrew McKenzie,³ and Martin Turner¹

Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme,¹ Laboratory of Molecular Neuroscience, The Babraham Institute, Babraham, Cambridge CB2 4AT,² Laboratory for Molecular Biology, Hills Road, Cambridge CB2 2QM, United Kingdom³

Received 25 March 2003/ Returned for modification 22 April 2003/ Accepted 20 October 2003

RhoG is a low-molecular-weight GTPase highly expressed in lymphocytes that activates gene transcription and promotes cytoskeletal reorganization in vitro. To study the in vivo function of RhoG, we generated mice homozygous for a targeted disruption of the RhoG gene. Despite the absence of RhoG, the development of B and T lymphocytes was unaffected. However, there was an increase in the level of serum immunoglobulin G1 (IgG1) and IgG2b as well as a mild increase of the humoral immune response to thymus-dependent antigens. In addition, B- and T-cell proliferation in response to antigen receptor cross-linking was slightly increased. Although RhoG deficiency produces a mild phenotype, our experiments suggest that RhoG may contribute to the negative regulation of immune responses. The lack of a strong phenotype could indicate a functional redundancy of RhoG with other Rac proteins in lymphocytes.

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* Corresponding author. Mailing address: Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom. Phone: 44 1223 496 545. Fax: 44 1223 496 023. E-mail: elena.vigorito{at}bbsrc.ac.uk.

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Molecular and Cellular Biology, January 2004, p. 719-729, Vol. 24, No. 2
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.2.719-729.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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