Figure 4. IL-10 inhibition of elongation at TNF is RelA dependent. (A and B) Cells were transfected with a siControl or siRelA oligonucleotides. Cells were stimulated with LPS with or without IL-10 for 1 h, after which ChIP was performed using RelA-specific antibodies and primers designed to the κB4 site of TNF (A) or Pol II–specific antibodies and primers specific for the TNF TSS or downstream regions (B). (C) Cells were treated with or without LPS for 1 h and ChIP was performed using Pol II–specific (left), phosphor-Ser2 (middle), or CDK9 (right) antibodies and primers specific for the TNF TSS+1. Data are expressed as mean ± SD of triplicate measurements for a single donor representative of three independent experiments using different donors.
Figure 4.

IL-10 inhibition of elongation at TNF is RelA dependent. (A and B) Cells were transfected with a siControl or siRelA oligonucleotides. Cells were stimulated with LPS with or without IL-10 for 1 h, after which ChIP was performed using RelA-specific antibodies and primers designed to the κB4 site of TNF (A) or Pol II–specific antibodies and primers specific for the TNF TSS or downstream regions (B). (C) Cells were treated with or without LPS for 1 h and ChIP was performed using Pol II–specific (left), phosphor-Ser2 (middle), or CDK9 (right) antibodies and primers specific for the TNF TSS+1. Data are expressed as mean ± SD of triplicate measurements for a single donor representative of three independent experiments using different donors.

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