| First Author | Kabra NH | Year | 2001 |
| Journal | Proc Natl Acad Sci U S A | Volume | 98 |
| Issue | 11 | Pages | 6307-12 |
| PubMed ID | 11353862 | Mgi Jnum | J:69617 |
| Mgi Id | MGI:1934999 | Doi | 10.1073/pnas.111158698 |
| Citation | Kabra NH, et al. (2001) T cell-specific FADD-deficient mice: FADD is required for early T cell development. Proc Natl Acad Sci U S A 98(11):6307-12 |
| abstractText | FADD/Mort1, initially identified as a Fas-associated death-domain containing protein, functions as an adapter molecule in apoptosis initiated by Fas, tumor necrosis factor receptor-I, DR3, and TRAIL-receptors. However, FADD likely participates in additional signaling cascades. FADD-null mutations in mice are embryonic-lethal, and analysis of FADD(-)/- T cells from RAG-1(-)/- reconstituted chimeras has suggested a role for FADD in proliferation of mature T cells. Here, we report the generation of T cell-specific FADD-deficient mice via a conditional genomic rescue approach. We find that FADD-deficiency leads to inhibition of T cell development at the CD4(-)CD8(-) stage and a reduction in the number of mature T cells. The FADD mutation does not affect apoptosis or the proximal signaling events of the pre-T cell receptor; introduction of a T cell receptor transgene fails to rescue the mutant phenotype. These data suggest that FADD, through either a death-domain containing receptor or a novel receptor-independent mechanism, is required for the proliferative phase of early T cell development. |
