| First Author | Schnell S | Year | 2006 |
| Journal | Blood | Volume | 108 |
| Issue | 2 | Pages | 591-9 |
| PubMed ID | 16569770 | Mgi Jnum | J:135744 |
| Mgi Id | MGI:3794392 | Doi | 10.1182/blood-2005-11-4616 |
| Citation | Schnell S, et al. (2006) Gimap4 accelerates T-cell death. Blood 108(2):591-9 |
| abstractText | Gimap4, a member of the newly identified GTPase of the immunity-associated protein family (Gimap), is strongly induced by the pre-T-cell receptor in precursor T lymphocytes, transiently shut off in double-positive thymocytes, and reappears after TCR-mediated positive selection. Here, we show that Gimap4 remains expressed constitutively in the cytosol of mature T cells. A C-terminal IQ domain binds calmodulin in the absence of calcium, and conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)- or PMA/ionomycin-induced PKC activation. To address the role of Gimap4 in T-cell physiology, we completed the genomic organization of the gimap4 locus and generated a Gimap4-null mutant mouse. Studies in these mice revealed no critical role of Gimap4 in T-cell development but in the regulation of apoptosis. We have found that Gimap4 accelerates the execution of programmed cell death induced by intrinsic stimuli downstream of caspase-3 activation and phosphatidylserine exposure. Apoptosis directly correlates with the phosphorylation status of Gimap4. |
