| First Author | Inoue H | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 313 |
| Issue | 1 | Pages | 125-8 |
| PubMed ID | 14672707 | Mgi Jnum | J:87752 |
| Mgi Id | MGI:3027651 | Doi | 10.1016/j.bbrc.2003.11.097 |
| Citation | Inoue H, et al. (2004) Negative regulation of hematopoiesis by the fused in myeloproliferative disorders gene product. Biochem Biophys Res Commun 313(1):125-8 |
| abstractText | The t(8;13) translocation, found in a rare and aggressive type of stem cell myeloproliferative disorder, leads to the generation of a fusion protein between the N-terminal gene product of fused in myeloproliferative disorders (FIM)/ZNF198 and the fibroblast growth factor receptor 1 (FGFR1) kinase domain. The chimeric protein was reported to have constitutively activated tyrosine kinase activity. However, little is known about a role of FIM in hematopoietic cell regulation. Here we show that FIM protein is ubiquitously expressed in mouse embryonic tissues but much less in hematopoietic cells. We also show that forced expression of FIM inhibits the emergence of hematopoietic cells in the cultured mouse aorta-gonad-mesonephros (AGM) region on embryonic day (E) 11.5, where definitive hematopoiesis is first found during embryogenesis. These results suggest that the expression level of FIM determines the development of hematopoiesis during mouse ontogeny. |
