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Evi-1 is a critical regulator for hematopoietic stem cells and transformed leukemic cells.

Evi-1 has been recognized as one of the dominant oncogenes associated with murine and human myeloid leukemia. Here, we show that hematopoietic stem cells (HSCs) in Evi-1-deficient embryos are severely reduced in number with defective proliferative and repopulating capacity. Selective ablation of Evi-1 in Tie2(+) cells mimics Evi-1 deficiency, suggesting that Evi-1 function is required in Tie2(+) hematopoietic stem/progenitors. Conditional deletion of Evi-1 in the adult hematopoietic system revealed that Evi-1-deficient bone marrow HSCs cannot maintain hematopoiesis and lose their repopulating ability. In contrast, Evi-1 is dispensable for blood cell lineage commitment. Evi-1(+/-) mice exhibit the intermediate phenotype for HSC activity, suggesting a gene dosage requirement for Evi-1. We further demonstrate that disruption of Evi-1 in transformed leukemic cells leads to significant loss of their proliferative activity both in vitro and in vivo. Thus, Evi-1 is a common and critical regulator essential for proliferation of embryonic/adult HSCs and transformed leukemic cells.

Pubmed ID: 18682242


  • Goyama S
  • Yamamoto G
  • Shimabe M
  • Sato T
  • Ichikawa M
  • Ogawa S
  • Chiba S
  • Kurokawa M


Cell stem cell

Publication Data

August 7, 2008

Associated Grants


Mesh Terms

  • Animals
  • Bone Marrow Cells
  • Cell Line, Transformed
  • Cell Lineage
  • Cell Proliferation
  • Cell Survival
  • DNA-Binding Proteins
  • Gene Dosage
  • Hematopoiesis
  • Hematopoietic Stem Cell Transplantation
  • Hematopoietic Stem Cells
  • Humans
  • Leukemia, Myeloid
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microarray Analysis
  • Proto-Oncogenes
  • Receptor, TIE-2
  • Transcription Factors