Fig. 3.
Fig. 3. In vivo footprinting analyses of the γ-globin gene promoter. (A) A sickle cell anemia patient (patient no. 8). Lane 1, hemin-induced K562; lane 2, before therapy; lane 3, during therapy; lane 4, naked DNA. (B) A β-thalassemia patient (patient no. 7). Lane 1, before therapy; lane 2, during therapy; lane 3, naked DNA. The location of the canonical elements is shown at the right of figures. (•) Footprinted G residues; (▴) G residues that showed hyperreactivity to DMS. The arrow indicates the location of three G residues that were footprinted in K562 cells but were not footprinted in patients’ samples.

In vivo footprinting analyses of the γ-globin gene promoter. (A) A sickle cell anemia patient (patient no. 8). Lane 1, hemin-induced K562; lane 2, before therapy; lane 3, during therapy; lane 4, naked DNA. (B) A β-thalassemia patient (patient no. 7). Lane 1, before therapy; lane 2, during therapy; lane 3, naked DNA. The location of the canonical elements is shown at the right of figures. (•) Footprinted G residues; (▴) G residues that showed hyperreactivity to DMS. The arrow indicates the location of three G residues that were footprinted in K562 cells but were not footprinted in patients’ samples.

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