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Download 1779-1790 March 30, 2017
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Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in hematopoietic stem/progenitor cells by Hiroyoshi Kunimoto, Anna Sophia McKenney, Cem Meydan, Kaitlyn Shank, Abbas Nazir, Franck Rapaport, Benjamin Durham, Francine E. Garrett-Bakelman, Elodie Pronier, Alan H. Shih, Ari Melnick, Jayanta Chaudhuri, and Ross L. Levine Blood Volume 129(13):1779-1790 March 30, 2017 ©2017 by American Society of Hematology Disrupted Aid expression and enzymatic activity in Aid knockout cells. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology Aid loss causes myeloid expansion and anemia in vivo. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology Ablation of Aid does not affect long-term HSC self-renewal but causes altered expression of Cebpa and Gata1 in myeloid progenitors. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology Aid loss does not cooperate with Tet2 loss in hematopoietic regulation. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology AID knockdown in human BM cells causes skewed differentiation toward myelomonocytic lineage. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology Deletion of Aid leads to transcriptional alteration of some key regulators of erythropoiesis and enhanced DNA methylation in gene regulatory elements. Hiroyoshi Kunimoto et al. Blood 2017;129:1779-1790 ©2017 by American Society of Hematology
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