Immunological Function in Mice Lacking the Rac-Related GTPase RhoG

AUTOR(ES)

Vigorito, Elena

FONTE

American Society for Microbiology

RESUMO

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.

Documentos Relacionados

• RhoG GTPase Controls a Pathway That Independently Activates Rac1 and Cdc42Hs
• Rac-Related GTP-Binding Protein in Elicitor-Induced Reactive Oxygen Generation by Suspension-Cultured Soybean Cells1
• Small GTPase RhoG Is a Key Regulator for Neurite Outgrowth in PC12 Cells
• SGEF, a RhoG Guanine Nucleotide Exchange Factor that Stimulates Macropinocytosis
• Kinectin Is a Key Effector of RhoG Microtubule-Dependent Cellular Activity