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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Masuoka, H. C. Articles by Townes, T. M. Search for Related Content PubMed PubMed Citation Articles by Masuoka, H. C. Articles by Townes, T. M. Related Collections Hematopoiesis and Stem Cells Red Cells Plenary Papers Gene Therapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 February 2002, Vol. 99, No. 3, pp. 736-745 PLENARY PAPER Targeted disruption of the activating transcription factor 4 gene results in severe fetal anemia in mice Howard C. Masuoka and Tim M. Townes From the Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham. Activating transcription factor (ATF) 4 is a ubiquitous basic leucine-zipper transcription factor that is a member of the ATF/cyclic adenosine monophosphate responsive element-binding (CREB) protein family. To determine the in vivo function of ATF4, the ATF4 gene in murine embryonic stem cells was deleted and homozygous mutant mice were generated. ATF4 null fetuses were severely anemic because of an impairment in fetal-liver definitive hematopoiesis; the hematocrit in 15.5-day mutant fetuses was 0.15, whereas that in controls was 0.35. The fetal livers in homozygous ATF4 mutants were pale and hypoplastic. In vitro culture of fetal-liver cells showed fewer hematopoietic progenitors per embryo and a dramatic decrease in the size of progenitor colonies. Culture of primary murine embryonic fibroblasts showed a proliferative defect. 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