Figure 6.
Figure 6. Analysis of leukocytes after CID administration. PCR primers were designed to flank the mutation responsible for the PK deficiency. The A>G transition results in the loss of a BstEII site (A, bold). DNA was purified from 50 μL peripheral blood from the experimental mice in Figure 4 at week 44. DNA was also obtained from the peripheral blood of CBA/N and CBA-Pk-1slc/Pk-1slc (pk) mice. This genomic DNA was used as a template for PCR. The resultant product was digested with BstEII and subjected to agarose gel electrophoresis (B). Relative donor contribution was determined based on band intensity (C). Fifty microliters peripheral blood was also used for flow cytometric analysis to determine GFP expression in the leukocytes. Forward and side scatter was used to identify the neutrophil and lymphocyte populations. Percentages of GFP expression in the 2 cell types did not differ significantly between CID-treated and untreated mice (D). Error bars indicate 1 standard deviation.

Analysis of leukocytes after CID administration. PCR primers were designed to flank the mutation responsible for the PK deficiency. The A>G transition results in the loss of a BstEII site (A, bold). DNA was purified from 50 μL peripheral blood from the experimental mice in Figure 4 at week 44. DNA was also obtained from the peripheral blood of CBA/N and CBA-Pk-1slc/Pk-1slc (pk) mice. This genomic DNA was used as a template for PCR. The resultant product was digested with BstEII and subjected to agarose gel electrophoresis (B). Relative donor contribution was determined based on band intensity (C). Fifty microliters peripheral blood was also used for flow cytometric analysis to determine GFP expression in the leukocytes. Forward and side scatter was used to identify the neutrophil and lymphocyte populations. Percentages of GFP expression in the 2 cell types did not differ significantly between CID-treated and untreated mice (D). Error bars indicate 1 standard deviation.

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