| First Author | Vigorito E | Year | 2004 |
| Journal | Mol Cell Biol | Volume | 24 |
| Issue | 2 | Pages | 719-29 |
| PubMed ID | 14701744 | Mgi Jnum | J:87580 |
| Mgi Id | MGI:3027214 | Doi | 10.1128/MCB.24.2.719-729.2004 |
| Citation | Vigorito E, et al. (2004) Immunological function in mice lacking the Rac-related GTPase RhoG. Mol Cell Biol 24(2):719-29 |
| abstractText | 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. |
