Prochemerin processing by factor XIa

distinct expression patterns regulated by the promoters (respectively, Vav promoter; long terminal repeat of retrovirus vector; and the authentic ASXL1 promoter).Another significant difference in the phenotypes of the Tg and locus KI mice is that the numbers of HSCs and progenitors are increased in the former but not in the latter, as are the common myeloid progenitor/ granulocyte-macrophage progenitor.Chimerism in competitive transplantation and the number of in vitro colonyforming unit cells are increased in the Tg model, but decreased in the locus KI mouse.Thus, as a model for clonal hematopoiesis or preleukemia, the locus KI mouse seems to be most appropriate.That notwithstanding, Yang's work deserves recognition for showing the first evidence for gain-of-function features of the ASXL1 mutations, which are frequently observed in myeloid malignancies and are always associated with poor prognosis.In addition, the present finding that BRD4 plays important roles in ASXL1 mutant-induced pathogenesis is clinically important and may pave a way to establishing a new strategy in treating the ASXL1 mutant-related hematological malignancies, including usage of HDAC inhibitors and the BRD4-bromodomain inhibitor JQ1, which inhibits BRD4 binding to chromatin.