作者: Christine Siligan , Dave N. T. Aryee , Robert Petermann , Heinrich Kovar , Johannes A. Schmid
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摘要: In 85% of Ewing family tumors, the NH 2 terminus EWS is fused to DNA-binding domain FLI1, an ets transcription factor. The resulting chimeric protein a strong transcriptional activator with transforming activity. We report that and EWS-FLI1 interact via their common COOH BARD1, putative tumor suppressor, in vitro vivo . Because BARD1 associates its -terminal RING breast cancer susceptibility gene BRCA1 provides platform for interactions proteins involved DNA repair checkpoint control, our results provide link between Ewing’s sarcoma product genome surveillance complex.