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GATA3 has been identified as a master regulator of T helper cells, as well as being important for early thymic progenitors and T-cell commitment. However, Gata3 expression initiates already at the hematopoietic stem cell (HSC) level, implicating a potential role also in the regulation of HSCs. Herein we used a conditional Gata3 knockout strategy in which Gata3 expression was completely deleted from the earliest stage of embryonic hematopoietic development after emergence of HSCs from hemogenic endothelium. Through a detailed analysis of HSCs at the phenotypic and functional level, we demonstrate that steady-state levels of HSCs are normal in Gata3(fl/fl)Vav-Cre(tg/+) mice. Moreover, through long-term primary and secondary transplantation experiments, we also unequivocally demonstrate that Gata3 has a redundant role in post-transplantation HSC self-renewal.

Original publication




Journal article



Publication Date





1291 - 1293


Animals, Cell Proliferation, Cells, Cultured, GATA3 Transcription Factor, Hematopoiesis, Hematopoietic Stem Cell Transplantation, Hematopoietic Stem Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Signal Transduction