Figure 2.
Figure 2. GPI isozyme analysis for the contribution by the knock-in ES clones to tissue in the chimera mice. (A) Schematic representation of the procedure for GPI analysis (see “Materials and methods”). (B) Representative results of the assay for chimera mice generated with knock-in clones for each of the AML1 mutant cDNAs. Lysates from tissues were separated by electrophoresis and stained for GPI activity. Contribution by ES cells is indicated by the GPI-A isoform, and that by host-derived cells is indicated by the GPI-B isoform. Results shown are for brain (Br), kidney (K), thymus (T), liver (L), spleen (Sp), bone marrow (BM), and peripheral blood (PB), with ES cells as GPI-A controls. (C) Columns with bars signifying standard deviation indicate quantification of tissue contributions by knock-in clones. Seven chimera mice were analyzed for full-length AML1 (WT: 451), 4 each for Δ446, Δ390, and Δ320, and 5 for Δ293 knock-in clones.

GPI isozyme analysis for the contribution by the knock-in ES clones to tissue in the chimera mice. (A) Schematic representation of the procedure for GPI analysis (see “Materials and methods”). (B) Representative results of the assay for chimera mice generated with knock-in clones for each of the AML1 mutant cDNAs. Lysates from tissues were separated by electrophoresis and stained for GPI activity. Contribution by ES cells is indicated by the GPI-A isoform, and that by host-derived cells is indicated by the GPI-B isoform. Results shown are for brain (Br), kidney (K), thymus (T), liver (L), spleen (Sp), bone marrow (BM), and peripheral blood (PB), with ES cells as GPI-A controls. (C) Columns with bars signifying standard deviation indicate quantification of tissue contributions by knock-in clones. Seven chimera mice were analyzed for full-length AML1 (WT: 451), 4 each for Δ446, Δ390, and Δ320, and 5 for Δ293 knock-in clones.

Close Modal

or Create an Account

Close Modal
Close Modal