AI Article Synopsis
- Ets-family genes are linked to leukemia and normal blood cell formation, with ERF being an ets-related gene that represses transcription and is regulated by MAPK phosphorylation.
- Using human cell lines, research showed that ERF promotes erythroid differentiation, indicated by increased levels of markers like CD71 and Glycophorin A, along with hemoglobin and GATA1.
- The ERF function is influenced by the MAPK pathway, with findings suggesting ERF plays a pivotal role in hematopoietic differentiation, contrasting with FLI1's effects and aligning with ETS1's role.
Article Abstract
Ets-family genes have been implicated in leukemia, as well as in normal hematopoiesis. ERF is an ets-related gene that represses transcription and is regulated by MAPK phosphorylation through its effect on ERF sub-cellular localization. Using pluripotent human cell lines, we studied the effect of ERF on erythroid differentiation. K562 and HEL cells expressing ERF expressed elevated levels of the erythroid-specific markers CD71 and Glycophorin A, as well as hemoglobin and GATA1. Treatment with the Erk kinase inhibitor PD98058 further enhanced the erythroid phenotype in ERF-expressing cells and cells expressing a non-phosphorylatable ERF mutant exhibited an even more enhanced phenotype. These results are consistent with the fact that ERF function is regulated by MAPK, and suggest that the effect of the MAPK pathway in erythroid differentiation is partially mediated by ERF. The effect of ERF is similar to the one shown for ETS1 and opposite to the FLI1 function in these cells, suggesting that several ets genes may play key roles in hematopoietic differentiation.
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