| First Author | Yu C | Year | 2002 |
| Journal | J Exp Med | Volume | 195 |
| Issue | 11 | Pages | 1387-95 |
| PubMed ID | 12045237 | Mgi Jnum | J:88711 |
| Mgi Id | MGI:3036946 | Doi | 10.1084/jem.20020656 |
| Citation | Yu C, et al. (2002) Targeted deletion of a high-affinity GATA-binding site in the GATA-1 promoter leads to selective loss of the eosinophil lineage in vivo. J Exp Med 195(11):1387-95 |
| abstractText | Transcription factor GATA-1 reprograms immature myeloid cells to three different hematopoietic lineages-erythroid cells, megakaryocytes, and eosinophils. GATA-1 is essential for maturation of erythroid and megakaryocytic precursors, as revealed by gene targeting in mice. Here we demonstrate that deletion of a high-affinity GATA-binding site in the GATA-1 promoter, an element presumed to mediate positive autoregulation of GATA-1 expression, leads to selective loss of the eosinophil lineage. These findings suggest that GATA-1 is required for specification of this lineage during hematopoietic development. Mice lacking the ability to produce eosinophils should prove useful in ascertaining the role of eosinophils in a variety of inflammatory or allergic disorders. |
