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. Author manuscript; available in PMC: 2016 Feb 15.
Published in final edited form as: J Immunol. 2015 Jan 21;194(4):1545–1554. doi: 10.4049/jimmunol.1402066

Figure 2.

Figure 2

cGAS is specifically induced by IFN-I in mouse and human macrophages. A, WT, Myd88−/−, and Trif−/− BMMs were stimulated with 100 ng/ml LPS for indicated time points, cGas mRNA level in these cells was detected by qPCR and normalized to Rpl32. B, WT, Cardif−/−, and Sting-gt/gt BMMs were transfected with 1 μg/ml polyI:C or polydA:dT for 4 h, cGas mRNA level in these cells was detected by qPCR and normalized to Rpl32. C, WT and Ifnar1−/− BMMs were transfected with indicated amount of cGAMP for 4 h, cGas mRNA level in these cells was detected by qPCR and normalized to Rpl32. D, THP-1-differentiated macrophages were treated with 500 U/ml human IFNα for indicated time points, RNA was extracted from these cells and cGAS mRNA level was detected by qPCR and normalized to RPL32. E, THP-1 cells were treated with indicated amount of human IFNα (10 to 1000 U/ml) for 4 h, RNA was extracted from these cells and cGAS mRNA level was detected by qPCR and normalized to RPL32. F, THP-1 cells were transfected with 1 μg/ml polyI:C or polydA:dT for 4 h, RNA was extracted from these cells and cGAS mRNA level was detected by qPCR and normalized to RPL32. G, THP-1 cells were treated with 500 U/ml human IFNα for indicated time points, cGAS protein level was detected by western blot. α-tubulin was shown as a loading control, *p<0.05, **p<0.01 (Student's t-test). Data of (A-F) are from three independent experiments (mean ± s.e.m). Data of (G) is one representative of three independent experiments.