Gain of function of ASXL1 truncating protein in the pathogenesis of myeloid malignancies
Key Points Transgenic expression of ASXL1aa1-587 truncating protein in the hematopoietic system leads to diverse myeloid malignancies in mice. ASXL1aa1-587 gains an interaction with BRD4 and Asxl1Y588XTg hematopoietic stem/progenitor cells are hypersensitive to BET bromodomain inhibitors.
