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. 2000 Aug 1;97(18):10162–10167. doi: 10.1073/pnas.160027697

Figure 4.

Figure 4

A52R and ΔMyD88 inhibit IL-1 signaling to NFκB. (A) Both A52R and ΔMyD88 inhibit the IL-1 but not the TNF pathway to NFκB. 293 cells were transfected with 300 ng of empty vector (EV; black bars), A52R (white bars), or ΔMyD88 (gray bars) for 24 h. At 6 h before harvesting, cells were stimulated with 100 ng/ml IL-1α or TNFα. NFκB reporter gene activity was then measured. (B) 293 cells were transfected with vectors encoding IL-1 signaling intermediates (150 ng each of IL-1RI and IL-1RAcP, 300 ng of IL-1RAcP or MyD88, or 150 ng of IRAK) together with 300 ng (or 450 ng for IRAK) of a vector encoding either A52R (Upper) or ΔMyD88 (Lower) for 24 h. NFκB reporter gene activity was then measured. (C) A52R inhibits IL-1-induced IL-8 promoter activation but not GH-induced lactogenesis hormone response element activation. (Left) HeLa cells were transfected with 10 ng of IL-1R1 and IL-1RAcP or MyD88 in the presence of 100 ng of empty vector (black bars) or vector encoding A52R (white bars). After 24–30 h, IL-8 promoter activity was measured by a reporter gene assay. (Right) HeLa cells were transfected with 100 ng of empty vector (black bar) or vector encoding A52R (white bar) 18 h before stimulation with 1 ng/ml growth hormone (GH) for 6 h. Lactogenesis hormone response element activity was measured by a reporter gene assay. Data are expressed as stimulation by GH over control in the absence or presence of A52R.