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. 2016 Oct 12;14(5):4505–4510. doi: 10.3892/mmr.2016.5825

Figure 3.

Figure 3.

NF-κB targeted TLR4 in chromatin and promotes TLR4 expression. (A) ChIP assay for NF-κB binding to TLR4 gene promoter. (B) Blocking NF-κB activation blocked TLR4 expression. (C) TLR4 protein expression in the cell membrane by FACS. Three group treatment: i) Mock group, LPS stimulation without any inhibitor; ii) STAT3 inhibitor group, LPS stimulation with STAT3 inhibitor; and iii) NF-κB inhibitor group, LPS stimulation with NF-κB inhibitor. LPS stimulation condition was 4 h and at 20 ng/ml LPS. STAT3 inhibitor was STA-21 (sc-200757; Santa Cruz Biotechnology, Inc.), 2 µmmol/l. NF-κB inhibitor was helenalin (sc-218579; Santa Cruz Biotechnology, Inc.), 5 µmmol/l. NF-κB, nuclear factor-κB; TLR4, Toll-like receptor 4; ChIP, chromatin immunoprecipitation; LPS, lipopolysaccharide.