| First Author | Tran DD | Year | 2005 |
| Journal | Immunity | Volume | 23 |
| Issue | 2 | Pages | 139-52 |
| PubMed ID | 16111633 | Mgi Jnum | J:100536 |
| Mgi Id | MGI:3588813 | Doi | 10.1016/j.immuni.2005.06.006 |
| Citation | Tran DD, et al. (2005) CAML is a p56Lck-interacting protein that is required for thymocyte development. Immunity 23(2):139-52 |
| abstractText | Calcium modulating cyclophilin ligand (CAML) is a ubiquitously expressed protein implicated in T cell signaling, although its mechanism and physiologic role in the immune system are unknown. We show here that CAML is essential for peripheral T cell development. Inactivation of CAML in mouse thymocytes lowered the numbers of double-positive and single-positive thymocytes, concomitant with reduced positive and enhanced negative selection. We found that CAML interacts with p56Lck and appears to regulate subcellular localization of the kinase in both resting and T cell receptor (TCR)-stimulated cells. CAML-deficient cells displayed enhanced p56lck and ZAP-70 phosphorylation and increased IL2 production and cell death after TCR stimulation, suggesting that CAML may act as a negative regulator of p56lck. Our data establish a novel role for CAML as an essential mediator of T cell survival during thymopoiesis and indicate that its loss deregulates p56Lck signaling. |
