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. 2003 Aug 18;198(4):521–531. doi: 10.1084/jem.20030701

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Copyright © 2003, The Rockefeller University Press

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Figure 8. — (A) Overexpression of WT (N), but not C877T mutant (M), IRAK-4 expression vector inhibits LPS- and IL-1–mediated signaling in HEK293T cells. Cells were transiently transfected as described in Fig. 7, permitted to recover for 48 h, and stimulated with medium, LPS, or rIL-1β for 5 h before measurement of NF-κB reporter activity. (B) Overexpression of WT (N), but not C877T mutant (M), IRAK-4 expression vectors differentially modulate IRAK-1 kinase activity. Cells were transiently transfected with control pCDNA3.1, pRK7-IRAK4 (N), or pRK7-IRAK4 (M; 5 μg per transfection). After 40 h recovery, cells were stimulated with rIL-1β for the indicated times, followed by lysis of cells and the IRAK-1 kinase assay (n = 3).

Figure 8. — (A) Overexpression of WT (N), but not C877T mutant (M), IRAK-4 expression vector inhibits LPS- and IL-1–mediated signaling in HEK293T cells. Cells were transiently transfected as described in Fig. 7, permitted to recover for 48 h, and stimulated with medium, LPS, or rIL-1β for 5 h before measurement of NF-κB reporter activity. (B) Overexpression of WT (N), but not C877T mutant (M), IRAK-4 expression vectors differentially modulate IRAK-1 kinase activity. Cells were transiently transfected with control pCDNA3.1, pRK7-IRAK4 (N), or pRK7-IRAK4 (M; 5 μg per transfection). After 40 h recovery, cells were stimulated with rIL-1β for the indicated times, followed by lysis of cells and the IRAK-1 kinase assay (n = 3).