Roles of leukemogenic oncogenes in the regulation of metabolism, growth, and differentiation of hematopoietic stem cells

1.RUNX1的C端缺失突变体RUNX1dC通过抑制Gadd45a2的表达，减弱了小鼠c-kit^+Sca-1^+Lin^-细胞对紫外线辐射的DNA损伤修复反应。FIP1L1-PDGFRpha不仅能促进KSL细胞的嗜酸性粒细胞祖细胞(EOPs)的发育，而且还能使其他细胞系的EOPs发生异常。3.BCR-ABL通过RAS/MAPK途径诱导p21^&lt；WAF1&GT；抑制红细胞生成，促进粒系生成。

1. The C-terminal deletion mutant of RUNX1, RUNX1dC, attenuates DNA-damage repair responses to UV irradiation in murine c-KIT^+Sca-1^+Lin^- cells by suppressing the expression of Gadd45a.2. FIP1L1-PDGFRalpha not only enhanced the development of eosinophil progenitors (EoPs) from KSL cells but also aberrantly developed EoPs from progenitors in other lineages.3.BCR-ABL inhibited erythropoiesis through the induction of p21^<WAF1> via Ras/MAPK, while it promoted granulopoiesis.