Figure 1
Figure 1. In vivo expansion of HSCs by AML1a expression. (A) Retrovirus vector (TetOFF-GFP-tetO-AML1a) allowing Dox-controllable expression of AML1a (not to scale). (B) Expression of AML1a in BM-derived hematopoietic cells infected with TetOFF-GFP-tetO-AML1a retrovirus, in the absence (0 hours) and after the addition of Dox at the indicated time. (C) Transplanted CRUs, and the fold-increase of CRUs after 4 or 3 (*) months in vivo after transplantation, are presented at the bottom. Corresponding CRUs after 4 or 3 (*) months in vivo are presented for vector-only virus (□) and TetOFF-GFP-tetO-AML1a–infected (■) cells. Bars represent 95% CIs. Results of 3 independent experiments each for the control and TetOFF-GFP-tetO-AML1a are presented.

In vivo expansion of HSCs by AML1a expression. (A) Retrovirus vector (TetOFF-GFP-tetO-AML1a) allowing Dox-controllable expression of AML1a (not to scale). (B) Expression of AML1a in BM-derived hematopoietic cells infected with TetOFF-GFP-tetO-AML1a retrovirus, in the absence (0 hours) and after the addition of Dox at the indicated time. (C) Transplanted CRUs, and the fold-increase of CRUs after 4 or 3 (*) months in vivo after transplantation, are presented at the bottom. Corresponding CRUs after 4 or 3 (*) months in vivo are presented for vector-only virus (□) and TetOFF-GFP-tetO-AML1a–infected (■) cells. Bars represent 95% CIs. Results of 3 independent experiments each for the control and TetOFF-GFP-tetO-AML1a are presented.

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