Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@article{AbdelWahab2013DeletionOA,
  title={Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo},
  author={O. Abdel-Wahab and Jie Gao and Mazhar Adli and A. Dey and T. Trimarchi and Y. Chung and C. Kuscu and Todd Hricik and Delphine Ndiaye-Lobry and Lindsay M. LaFave and R. Koche and A. Shih and O. Guryanova and Eunhee Kim and S. Li and Suveg Pandey and J. Shin and L. Telis and Jinfeng Liu and P. Bhatt and S. Monette and X. Zhao and C. Mason and Christopher Y Park and B. Bernstein and I. Aifantis and R. Levine},
  journal={The Journal of Experimental Medicine},
  year={2013},
  volume={210},
  pages={2641 - 2659}
}
Loss of Asxl1 results in myelodysplastic syndrome, whereas concomitant deletion of Tet2 restores HSC self-renewal and triggers a more severe disease phenotype distinct from that seen in single-gene knockout mice. 
Disruption of asxl1 results in myeloproliferative neoplasms in zebrafish
Dose-dependent role of the cohesin complex in normal and malignant hematopoiesis
The distinct biological implications of Asxl1 mutation and its roles in leukemogenesis revealed by a knock-in mouse model
ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion
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Ten-Eleven-Translocation 2 (TET2) negatively regulates homeostasis and differentiation of hematopoietic stem cells in mice
ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression.
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