| First Author | Hobbs NK | Year | 2002 |
| Journal | Cell | Volume | 110 |
| Issue | 1 | Pages | 43-54 |
| PubMed ID | 12150996 | Mgi Jnum | J:77714 |
| Mgi Id | MGI:2182475 | Doi | 10.1016/s0092-8674(02)00806-1 |
| Citation | Hobbs NK, et al. (2002) Removing the Vertebrate-Specific TBP N Terminus Disrupts Placental beta2m-Dependent Interactions with the Maternal Immune System. Cell 110(1):43-54 |
| abstractText | Mammalian TBP consists of a 180 amino acid core that is common to all eukaryotes, fused to a vertebrate-specific N-terminal domain. We generated mice having a modified tbp allele, tbp(DeltaN), that produces a version of TBP lacking 111 of the 135 vertebrate-specific amino acids. Most tbp(DeltaN/DeltaN) fetuses (>90%) died in midgestation from an apparent defect in the placenta. tbp(DeltaN/DeltaN) fetuses could be rescued by supplying them with a wild-type tetraploid placenta. Mutants also could be rescued by rearing them in immunocompromised mothers. In immune-competent mothers, survival of tbp(DeltaN/DeltaN) fetuses increased when fetal/placental beta2m expression was genetically disrupted. These results suggest that the TBP N terminus functions in transcriptional regulation of a placental beta2m-dependent process that favors maternal immunotolerance of pregnancy. |
