| First Author | Khalaf WF | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 9 | Pages | 3538-41 |
| PubMed ID | 15644420 | Mgi Jnum | J:105055 |
| Mgi Id | MGI:3613346 | Doi | 10.1182/blood-2004-05-2021 |
| Citation | Khalaf WF, et al. (2005) K-Ras is essential for normal fetal liver erythropoiesis. Blood 105(9):3538-41 |
| abstractText | In vitro studies suggest that Ras activation is necessary for erythroid cell development. However, genetic inactivation of the Ras isoforms H-Ras, N-Ras, and K-Ras in mice reportedly did not affect adult or fetal erythropoiesis, though K-Ras(-/-) embryos were anemic. Given these discrepancies, we performed a more detailed analysis of fetal erythropoiesis in K-Ras(-/-) embryos. Day-13.5 K-Ras(-/-) embryos were pale with a marked reduction of mature erythrocytes in their fetal livers. The frequency and number of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony-forming unit [CFU-E]) were reduced in K-Ras(-/-) fetal livers compared with wild-type controls and displayed a delay in terminal erythroid cell maturation. Further, K-Ras(-/-) hematopoietic progenitors had reduced proliferation in response to erythropoietin and Kit ligand compared with control cells. Thus, these studies identify K-Ras as a unique Ras isoform that is essential for regulating fetal erythropoiesis in vivo. |
