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. Author manuscript; available in PMC: 2012 Jun 16.
Published in final edited form as: Cell Host Microbe. 2011 Jun 16;9(6):496–507. doi: 10.1016/j.chom.2011.05.006

Figure 3. Type-I IFN signaling induces expression of RIP2.

Figure 3

(A) BMDMs from WT mice were treated with poly I:C, DMXAA, or IFN-β for the indicated times, and cell extracts were assessed for RIP2 and α-tubulin levels by immunoblotting. (B) BMDMs from WT, Trif−/−Ips1−/−, and Ifnar1−/− mice were treated with poly I:C, DMXAA, or IFN-β for 24 h, and cell extracts were assessed for RIP2 and α-tubulin levels by immunoblotting. (C) BMDMs from WT mice were treated with poly I:C, DMXAA, or IFN-β for the indicated times, and total RNA was isolated to analyze for Nod1 and Nod2 expression. Gene expression was normalized to that of β-actin. (D) BMDMs from WT, Trif−/−Ips1−/−, and Ifnar1−/− mice were treated with poly I:C, DMXAA, or IFN-β for 8 h, and total RNA was isolated to analyze expression of Nod1 and Nod2. * p < 0.05, *** p < 0.001, comparison between untreated and treated macrophage cultures. Results are representative of 2 or 3 independent experiments.

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