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Removing the vertebrate-specific TBP N terminus disrupts placental beta2m-dependent interactions with the maternal immune system.

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Resource Type

  1. Journal article


  1. Resource Description
    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.
  2. Author
    Schmidt, Ed
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  4. PubMed ID
Provenance Metadata About This Resource Record
  1. workflow state
  2. contributor
    qking (Quinton King)
  3. created
  4. creator
    qking (Quinton King)
  5. modified
Copyright © 2016 by the President and Fellows of Harvard College
The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016