Fig. 3.
Fig. 3. The tandem MAREs of HS2 are necessary for the interaction of NF-E2 with HS2. / (A) Structure of the HS2(Gal4)5.1γluciferase reporter construct stably integrated into K562 cells. HS2 was separated from the Aγ-globin promoter by a 5.1 kilobase (kb) phage lambda MluI fragment (5.1 λ). (B) Ethidium bromide-stained agarose gels of input chromatin (left panel) and PCR products of samples using primers specific for the mutated HS2 lacking MAREs, the Aγ-globin promoter, and IgH from a representative experiment. The immunoprecipitation conditions are indicated below each lane. No antibody, No Ab; anti-p45 polyclonal sera, p45; preimmune sera, PI; no chromatin, No Chr. (C) Relative intensity of PCR products from at least 3 independent experiments (mean ± SEM). The signal obtained with 0.02% of input was set to 1.

The tandem MAREs of HS2 are necessary for the interaction of NF-E2 with HS2.

(A) Structure of the HS2(Gal4)5.1γluciferase reporter construct stably integrated into K562 cells. HS2 was separated from the Aγ-globin promoter by a 5.1 kilobase (kb) phage lambda MluI fragment (5.1 λ). (B) Ethidium bromide-stained agarose gels of input chromatin (left panel) and PCR products of samples using primers specific for the mutated HS2 lacking MAREs, the Aγ-globin promoter, and IgH from a representative experiment. The immunoprecipitation conditions are indicated below each lane. No antibody, No Ab; anti-p45 polyclonal sera, p45; preimmune sera, PI; no chromatin, No Chr. (C) Relative intensity of PCR products from at least 3 independent experiments (mean ± SEM). The signal obtained with 0.02% of input was set to 1.

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