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

eagle-i ID

http://montana.eagle-i.net/i/0000012e-59d7-1f48-55f8-6fb280000000

Resource Type

  1. Journal article

Properties

  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
  3. Website(s)
    http://www.ncbi.nlm.nih.gov/pubmed?term=12150996
  4. PubMed ID
    12150996
 
RDFRDF
 
Provenance Metadata About This Resource Record
  1. workflow state
    Published
  2. contributor
    qking (Quinton King)
  3. created
    2011-02-24T16:44:26.995-06:00
  4. creator
    qking (Quinton King)
  5. modified
    2011-04-29T13:51:37.310-05:00

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