Nature Communications (Jul 2018)
Mutant ASXL1 cooperates with BAP1 to promote myeloid leukaemogenesis
- Shuhei Asada,
- Susumu Goyama,
- Daichi Inoue,
- Shiori Shikata,
- Reina Takeda,
- Tsuyoshi Fukushima,
- Taishi Yonezawa,
- Takeshi Fujino,
- Yasutaka Hayashi,
- Kimihito Cojin Kawabata,
- Tomofusa Fukuyama,
- Yosuke Tanaka,
- Akihiko Yokoyama,
- Satoshi Yamazaki,
- Hiroko Kozuka-Hata,
- Masaaki Oyama,
- Shinya Kojima,
- Masahito Kawazu,
- Hiroyuki Mano,
- Toshio Kitamura
Affiliations
- Shuhei Asada
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Susumu Goyama
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Daichi Inoue
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Shiori Shikata
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Reina Takeda
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Tsuyoshi Fukushima
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Taishi Yonezawa
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Takeshi Fujino
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Yasutaka Hayashi
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Kimihito Cojin Kawabata
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Tomofusa Fukuyama
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Yosuke Tanaka
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- Akihiko Yokoyama
- National Cancer Center Tsuruoka Metabolomics Laboratory
- Satoshi Yamazaki
- Division of Stem Cell Therapy, The Institute of Medical Science, The University of Tokyo
- Hiroko Kozuka-Hata
- Medical Proteomics Laboratory, The Institute of Medical Science, The University of Tokyo
- Masaaki Oyama
- Medical Proteomics Laboratory, The Institute of Medical Science, The University of Tokyo
- Shinya Kojima
- Department of Cellular Signaling, Graduate School of Medicine, The University of Tokyo
- Masahito Kawazu
- Department of Medical Genomics, Graduate School of Medicine, The University of Tokyo
- Hiroyuki Mano
- Department of Cellular Signaling, Graduate School of Medicine, The University of Tokyo
- Toshio Kitamura
- Division of Cellular Therapy, Advanced Clinical Research Center, and Division of Stem Cell Signaling, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, The University of Tokyo
- DOI
- https://doi.org/10.1038/s41467-018-05085-9
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 18
Abstract
ASXL1 gene is often mutated in myeloid malignancies. Here, the authors show that mutant ASXL1 and BAP1 are in a positive feedback loop such that BAP1 induces monoubiquitination of mutant ASXL1, which in turn enhances BAP1 activity to potentiate myeloid transformation via HOXA clusters and IRF8.
