| First Author | Chae HD | Year | 2010 |
| Journal | PLoS One | Volume | 5 |
| Issue | 11 | Pages | e13970 |
| PubMed ID | 21103055 | Mgi Jnum | J:223715 |
| Mgi Id | MGI:5660102 | Doi | 10.1371/journal.pone.0013970 |
| Citation | Chae HD, et al. (2010) RhoH regulates subcellular localization of ZAP-70 and Lck in T cell receptor signaling. PLoS One 5(11):e13970 |
| abstractText | RhoH is an hematopoietic-specific, GTPase-deficient Rho GTPase that plays a role in T development. We investigated the mechanisms of RhoH function in TCR signaling. We found that the association between Lck and CD3zeta was impaired in RhoH-deficient T cells, due to defective translocation of both Lck and ZAP-70 to the immunological synapse. RhoH with Lck and ZAP-70 localizes in the detergent-soluble membrane fraction where the complex is associated with CD3zeta phosphorylation. To determine if impaired translocation of ZAP-70 was a major determinant of defective T cell development, Rhoh(-/-) bone marrow cells were transduced with a chimeric myristoylation-tagged ZAP-70. Myr-ZAP-70 transduced cells partially reversed the in vivo defects of RhoH-associated thymic development and TCR signaling. Together, our results suggest that RhoH regulates TCR signaling via recruitment of ZAP-70 and Lck to CD3zeta in the immunological synapse. Thus, we define a new function for a RhoH GTPase as an adaptor molecule in TCR signaling pathway. |
