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Publication : Arrest in primitive erythroid cell development caused by promoter-specific disruption of the GATA-1 gene.

First Author  Takahashi S Year  1997
Journal  J Biol Chem Volume  272
Issue  19 Pages  12611-5
PubMed ID  9139715 Mgi Jnum  J:40321
Mgi Id  MGI:87662 Doi  10.1074/jbc.272.19.12611
Citation  Takahashi S, et al. (1997) Arrest in primitive erythroid cell development caused by promoter-specific disruption of the GATA-1 gene. J Biol Chem 272(19):12611-5
abstractText  To elucidate the in vivo function of GATA-1 during hematopoiesis, we specifically disrupted the erythroid promoter of the GATA-1 gene in embryonic stem cells and generated germ line chimeras. Male offspring of chimeras bearing the targeted mutation were found to die by 12.5 days post coitus due to severe anemia while heterozygous females displayed characteristics ranging from severe anemia to normal erythropoiesis. When female heterozygotes were crossed with transgenic males carrying a reporter gene, which specifically marks primitive erythroid progenitors, massive accumulation of undifferentiated erythroid cells were observed in the yolk sacs of the GATA-1-mutant embryos, demonstrating that GATA-1 is required for the terminal differentiation of primitive erythroid cells in vivo.
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