| First Author | Chrétien S | Year | 1997 |
| Journal | Oncogene | Volume | 15 |
| Issue | 16 | Pages | 1995-9 |
| PubMed ID | 9365246 | Mgi Jnum | J:43802 |
| Mgi Id | MGI:1098960 | Doi | 10.1038/sj.onc.1201364 |
| Citation | Chretien S, et al. (1997) Abnormal erythropoietin (Epo) gene expression in the murine erythroleukemia IW32 cells results from a rearrangement between the G-protein beta2 subunit gene and the Epo gene. Oncogene 15(16):1995-9 |
| abstractText | Abnormal production of erythropoietin (Epo) has been described in several human and murine erythroleukemia. The murine IW32 cell line is derived from an F-MuLV-induced erythroleukemia. An autocrine Epo production due to the rearrangement of one Epo allele has been previously described (Beru et al., 1989). However, the exact mechanism leading to the transcriptional activation of the abnormal Epo gene was unknown. In this study, we show that this deregulated expression results from a deletion within chromosome 5. The Epo gene in the abnormal allele is under the control of the G-protein beta2 subunit gene promoter and the expressed mRNA results from the fusion of the non coding exon 1 of the G-protein beta2 subunit gene to a truncated Epo exon 1 gene. This resulting abnormal cDNA allows the expression of a normal Epo protein. |
