| First Author | Longmore GD | Year | 1991 |
| Journal | Cell | Volume | 67 |
| Issue | 6 | Pages | 1089-102 |
| PubMed ID | 1662116 | Mgi Jnum | J:1629 |
| Mgi Id | MGI:50156 | Doi | 10.1016/0092-8674(91)90286-8 |
| Citation | Longmore GD, et al. (1991) An activating mutation in the murine erythropoietin receptor induces erythroleukemia in mice: a cytokine receptor superfamily oncogene. Cell 67(6):1089-102 |
| abstractText | A point mutation at codon 129 of the murine erythropoietin receptor (cEpoR) results in constitutive activation. We have generated a recombinant spleen focus-forming retrovirus in which the env gene is replaced by the cEpoR cDNA. Mice infected with this virus (but not by viruses expressing the wild-type EpoR) develop erythrocytosis and splenomegaly. From the spleen of infected animals we have isolated clonal, growth factor-independent, proerythroblast cell lines that express cEpoR, do not express the putative oncogene spi-1, and have rearranged and inactivated expression of the p53 suppressor oncogene. These cells induce erythroleukemia upon injection into mice. This demonstrates that oncogenic point mutations exist in a member of the cytokine receptor superfamily. The activated erythropoietin receptor does not transform cultured fibroblasts, suggesting why oncogenic mutations in other members of this receptor superfamily have not been detected. |
