Figure 5
Figure 5. Genetic loss of Tr2/Tr4 abolishes the chromatin occupancy of TR2/TR4 and their cofactors at the DR-binding sites in the embryonic globin gene promoters. The binding of TR2/TR4 and other corepressors to select murine β-like globin gene promoters: εy (A), βh1 (B), and βmaj (C) as well as to an irrelevant control sequence located 5.9 kbp 5′ to the βmaj promoter (D) in infected Lin− cells were analyzed in ChIP experiments. Statistically significant enrichment of the orphan receptors and/or the cofactors at the promoters and control sequence is indicated in comparison with the control IgG values (indicated with asterisks; *P < .05).

Genetic loss of Tr2/Tr4 abolishes the chromatin occupancy of TR2/TR4 and their cofactors at the DR-binding sites in the embryonic globin gene promoters. The binding of TR2/TR4 and other corepressors to select murine β-like globin gene promoters: εy (A), βh1 (B), and βmaj (C) as well as to an irrelevant control sequence located 5.9 kbp 5′ to the βmaj promoter (D) in infected Lin cells were analyzed in ChIP experiments. Statistically significant enrichment of the orphan receptors and/or the cofactors at the promoters and control sequence is indicated in comparison with the control IgG values (indicated with asterisks; *P < .05).

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