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Fig. 3 | Arthritis Research & Therapy

Fig. 3

From: Mitochondrial protein CMPK2 regulates IFN alpha-enhanced foam cell formation, potentially contributing to premature atherosclerosis in SLE

Fig. 3

Signaling pathways involved in the activation and regulation of CMPK2. BMDMs were treated with different doses of IFN-α, IFN-γ, thrombin, lipopolysaccharide (LPS), Pam3CSK4, Poly(I:C), IL-1β, CpG ODN1826, or CpG ODN1585, and the expression of CMPK2 mRNA was measured by qPCR (a). The mRNA expression of CMPK2, SR-A, and ABCG1 was determined in TDMs treated with different doses of IFN-α (b). TDMs treated with 100 U/ml IFN-α were collected at different time points, and the protein levels of CMPK2, SR-A, and actin were measured by Western blotting (c). TDMs pretreated for 2 h with different doses of chemical compounds, including LY294002, PD98059, SP600125, SB203580, AG490, ruxolitinib, BMS-986165, or DMSO, were also treated with IFN-α for 24 h, and then, the cells were collected for the determination of CMPK2 mRNA by qPCR (D, left part) and in part by Western blotting (d, right part), respectively. Asterisks indicate values that are significantly different from the relevant control (*P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001)

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