The authors show that IGF-1-activated AKT leads to phosphorylation of EGR1 followed by sumoylation of EGR1 by ARF thereby producing a new modified molecule that directly transactivates the PTEN promoter.
The role of different erythropoietin receptor substructures for the activation of Egr-1 and the functional consequences of Egr-1 overexpression in the erythroleukemic cell line ELM-I-1 is analysed.
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