Ring1A and Ring1B inhibit expression of Glis2 to maintain murine MOZ-TIF2 AML stem cells

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  • Haruko Shima
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Emi Takamatsu-Ichihara
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Mika Shino
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Kazutsune Yamagata
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Takuo Katsumoto
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Yukiko Aikawa
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Shuhei Fujita
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;
  • Haruhiko Koseki
    RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan
  • Issay Kitabayashi
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan;

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<jats:title>Key Points</jats:title><jats:p>MOZ-TIF2 AML cells harboring deletion of Ring1A/B lose self-renewal capacity. Gli-similar 2 promotes differentiation of MOZ-TIF2 AML cells and is derepressed in Ring1A/B-knockout cells.</jats:p>

Journal

  • Blood

    Blood 131 (16), 1833-1845, 2018-04-19

    American Society of Hematology

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