Article summaryβ-Catenin is frequently dysregulated in acute myeloid leukemia (AML) and protein interactions govern its stability, localisation and activity, but these are poorly defined in AML.This study shows for the first time that β-catenin and Wilms tumour protein (WT1) interact and influence each other’s expression level and signalling activity in AML cells, which could inform future therapeutic strategies.
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