| First Author | Yu H | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 7 | Pages | 915-26 |
| PubMed ID | 11581314 | Mgi Jnum | J:119437 |
| Mgi Id | MGI:3702218 | Doi | 10.1084/jem.194.7.915 |
| Citation | Yu H, et al. (2001) Deficiency of small GTPase Rac2 affects T cell activation. J Exp Med 194(7):915-26 |
| abstractText | Rac2 is a hematopoietic-specific GTPase acting as a molecular switch to mediate both transcriptional activation and cell morphological changes. We have examined the effect of Rac2 deficiency during T cell activation. In Rac2(-/-) T cells, proliferation was reduced upon stimulation with either plate-bound anti-CD3 or T cell receptor-specific antigen. This defect is accompanied with decreased activation of mitogen activated protein kinase extracellular signal-regulated kinase (ERK)1/2 and p38, and reduced Ca(2)+ mobilization. TCR stimulation-induced actin polymerization is also reduced. In addition, anti-CD3 cross-linking-induced T cell capping is reduced compared with wild-type T cells. These results indicate that Rac2 is important in mediating both transcriptional and cytoskeletal changes during T cell activation. The phenotypic similarity of Rac2(-/-) to Vav(-/-) cells implicates Rac2 as a downstream mediator of Vav signaling. |
