| First Author | Waga K | Year | 2003 |
| Journal | Oncogene | Volume | 22 |
| Issue | 1 | Pages | 59-68 |
| PubMed ID | 12527908 | Mgi Jnum | J:81403 |
| Mgi Id | MGI:2449254 | Doi | 10.1038/sj.onc.1206072 |
| Citation | Waga K, et al. (2003) Leukemia-related transcription factor TEL accelerates differentiation of Friend erythroleukemia cells. Oncogene 22(1):59-68 |
| abstractText | TEL belongs to a member of the ETS family transcription factors that represses transcription of target genes such as FLI-1. Although TEL is essential for establishing hematopoiesis in neonatal bone marrow, its role in erythroid lineage is not understood. To investigate a role for TEL in erythroid differentiation, we introduced TEL into mouse erythroleukemia (MEL) cells. Overexpressing wild-type-TEL in MEL cells enhanced differentiation induced by hexamethylene bisacetamide or dimethylsulfoxide, as judged by the increased levels of erythroid-specific delta-aminolevulinate synthase and beta-globin mRNAs. TEL bound to a corepressor mSin3A through the helix-loop-helix domain. A TEL mutant lacking this domain still bound to the ETS binding site, but lost its transrepressional effect. This mutant completely blocked erythroid differentiation in MEL cells. Moreover, it showed dominant-negative effects over TEL-mediated transcriptional repression and acceleration of erythroid differentiation. Endogenous TEL mRNA was found to increase during the first 3 days in differentiating MEL cells and drastically decrease thereafter. All these data suggest that TEL might play some role in erythroid cell differentiation. |
