Article summary
β-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.
Competing Interest Statement
The authors have declared no competing interest.
Copyright
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.