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Publication : Mice lacking the transcriptional corepressor TIF1beta are defective in early postimplantation development.

First Author  Cammas F Year  2000
Journal  Development Volume  127
Issue  13 Pages  2955-63
PubMed ID  10851139 Mgi Jnum  J:62628
Mgi Id  MGI:1859236 Doi  10.1242/dev.127.13.2955
Citation  Cammas F, et al. (2000) Mice lacking the transcriptional corepressor TIF1beta are defective in early postimplantation development. Development 127(13):2955-63
abstractText  TIF1beta, a member of the transcriptional intermediary factor 1 family, has been reported to function as a corepressor for the large class of KRAB domain-containing zinc finger proteins of the Kruppel type. To address the biological function of TIF1beta, we have generated TIF1beta-deficient mice by gene disruption. TIF1beta protein was detected in wild-type but not TIF1beta(-/-) blastocysts. Homozygous mutant embryos, which developed normally until the blastocyst stage and underwent uterine implantation, were arrested in their development at the early egg-cylinder stage at about embryonic day (E) 5.5 and were completely resorbed by E8.5. Taken together, these results provide genetic evidence that TIF1beta is a developmental regulatory protein that exerts function(s) essential for early postimplantation development.
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