Skip to main content
. 2020 Mar 16;9:e52241. doi: 10.7554/eLife.52241

Figure 5. Subsets of genes induced by hyperosmotic stress are transcriptionally controlled by NF-κB c-Rel and TonEBP.

(A) TonEBP targets identified by literature demonstrate a general increase at mild intensity and decrease at high intensity hyperosmotic stress. (B–D) MEFs deficient in NF-κB c-Rel, NF-κB p65, and TonEBP were treated with the indicated stress intensity. RNA was isolated, and mRNA transcript levels analyzed via RT-qPCR. (E) Genes were categorized based on targeting of Rel-homology domain transcription factor complexes. (F) MEFs deficient in PACT were treated with the indicated stress intensity. RNA was isolated, and mRNA transcript levels analyzed via RT-qPCR.

Figure 5—source data 1. Graph values for RT-qPCR experiments in Figure 5.

Figure 5.

Figure 5—figure supplement 1. Additional proinflammatory gene expression programs are also dependent on PACT.

Figure 5—figure supplement 1.

(A) MEFs deficient in PACT were treated with the indicated stress intensity. RNA was isolated, and mRNA transcript levels analyzed via RT-qPCR.