Figure 7
Figure 7. Two pathways for activation of NF-κB target genes. In unstimulated cells, expression of NF-κB–regulated genes is often repressed by recruitment of HDACs by p50:p50 homodimers bound to nuclear κB sites (top). Canonical NF-κB stimulation results in displacement of p50 homodimers, binding of p65:p50 heterodimers, and recruitment of coactivators to chromatin (top). Alternatively, C/EBPs or C/EBPα AML mutants displace HDACs bound to p50 homodimers, resulting in activation of NF-κB–regulated gene independent of activation of the NF-κB system (bottom).

Two pathways for activation of NF-κB target genes. In unstimulated cells, expression of NF-κB–regulated genes is often repressed by recruitment of HDACs by p50:p50 homodimers bound to nuclear κB sites (top). Canonical NF-κB stimulation results in displacement of p50 homodimers, binding of p65:p50 heterodimers, and recruitment of coactivators to chromatin (top). Alternatively, C/EBPs or C/EBPα AML mutants displace HDACs bound to p50 homodimers, resulting in activation of NF-κB–regulated gene independent of activation of the NF-κB system (bottom).

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