| First Author | Huddleston H | Year | 2003 |
| Journal | Blood | Volume | 102 |
| Issue | 1 | Pages | 142-5 |
| PubMed ID | 12623844 | Mgi Jnum | J:106371 |
| Mgi Id | MGI:3618416 | Doi | 10.1182/blood-2002-10-3245 |
| Citation | Huddleston H, et al. (2003) Functional p85alpha gene is required for normal murine fetal erythropoiesis. Blood 102(1):142-5 |
| abstractText | In vitro studies suggest that activation of class IA phosphatidylinositol 3 (PI-3) kinase is necessary for normal erythroid cell development. However, when class IA PI-3 kinase-deficient mice were generated by a targeted deletion of the p85alpha regulatory subunit, fetal erythropoiesis was reportedly unaffected. Given the discrepancies between these studies, we performed a more detailed in vivo analysis of class IA PI-3 kinase-deficient embryos. Day-14.5 p85alpha-/- embryos are pale with a marked reduction of mature erythrocytes in their peripheral blood. Further, the absolute number and frequency of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony-forming unit [CFU-E]) are reduced in p85alpha-/- fetal livers compared with wild-type controls, which is associated with reduced proliferation. Taken together, these data establish an important role for p85alpha and class IA PI-3 kinase in regulating the development of both early and late erythroid progenitors in fetal liver. |
