Fig. 6.
Fig. 6. IL-10 does not block IFN-γ–induced STAT-1α binding to the ICAM-1 IRE. (A) Nuclear extracts from monocytes stimulated with IFN-γ (100 U/mL) in the presence (lanes 4 to 6) or absence of IL-10 (100 U/mL) (lanes 1 to 3) were incubated with anti–STAT-1α or anti–fos B antibody. (B) Nuclear extracts from monocytes stimulated with IFN-γ (100 U/mL) (lanes 1 to 4) and IL-10 (100 U/mL) (lanes 5 to 8) were incubated with anti–STAT-1α, anti–STAT-3, or both antibodies combined. Antibody binding complexes were assessed by gel mobility supershift with labeled ICAM-1 IRE. Data are representative of 3 experiments.

IL-10 does not block IFN-γ–induced STAT-1α binding to the ICAM-1 IRE. (A) Nuclear extracts from monocytes stimulated with IFN-γ (100 U/mL) in the presence (lanes 4 to 6) or absence of IL-10 (100 U/mL) (lanes 1 to 3) were incubated with anti–STAT-1α or anti–fos B antibody. (B) Nuclear extracts from monocytes stimulated with IFN-γ (100 U/mL) (lanes 1 to 4) and IL-10 (100 U/mL) (lanes 5 to 8) were incubated with anti–STAT-1α, anti–STAT-3, or both antibodies combined. Antibody binding complexes were assessed by gel mobility supershift with labeled ICAM-1 IRE. Data are representative of 3 experiments.

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