Fig. 5.
Fig. 5. The c-kithi population is absent from the fetal liver and AGM of embryos heterozygous for the knock-in. / Cbfb-MYH11 (Cbfb+/MYH11). (A) Cells were isolated from 11.5-dpc fetal liver ofCbfb+/+ (+/+),Cbfb+/MYH11 (+/MYH11), andCbfbGFP/MYH11 (GFP/MYH11) embryos and stained with anti–c-kit PE. Representative contour plots show the distribution of cells with respect to GFP and c-kit fluorescence. Cells were isolated from (B) fetal liver and (C) AGM ofCbfb+/+, and Cbfb+/MYH1111.5-dpc embryos and stained with PE-conjugated anti–c-kit and FITC-conjugated anti-CD34. Representative contour plots show the distribution of cells with respect to FITC and c-kit fluorescence.

The c-kithi population is absent from the fetal liver and AGM of embryos heterozygous for the knock-in

Cbfb-MYH11 (Cbfb+/MYH11). (A) Cells were isolated from 11.5-dpc fetal liver ofCbfb+/+ (+/+),Cbfb+/MYH11 (+/MYH11), andCbfbGFP/MYH11 (GFP/MYH11) embryos and stained with anti–c-kit PE. Representative contour plots show the distribution of cells with respect to GFP and c-kit fluorescence. Cells were isolated from (B) fetal liver and (C) AGM ofCbfb+/+, and Cbfb+/MYH1111.5-dpc embryos and stained with PE-conjugated anti–c-kit and FITC-conjugated anti-CD34. Representative contour plots show the distribution of cells with respect to FITC and c-kit fluorescence.

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