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Fig. 4 | Arthritis Research & Therapy

Fig. 4

From: N6-methyladenosine-dependent modification of circGARS acts as a new player that promotes SLE progression through the NF-κB/A20 axis

Fig. 4

MiR-19a-3p regulated the expression of YTHDF2 by targeting its mRNA 3′-UTR. a The degree of global m6A RNA methylation level of total RNA in 36 SLE samples was higher than that of the 25 healthy controls (P < 0.05). b Predicted the potential miRNAs targeting the 3′-UTR of YTHDF2 by TargetScan, and miR-19a had binding sites for YTHDF2. c WB (Western blot) analysis demonstrated that miR-19a-3p could significantly inhibit the expression of YTHDF2 in PBMCs, suggesting that miR-19a-3p is involved in the regulation of YTHDF2 mRNA. d Schematic diagram of the binding sites of miR-19a-3p in the 3′-UTR of YTHDF2 mRNA. The mutant was produced at the 3′-UTR of YTHDF2 mRNA. The 3′-UTR sequence of the YTHDF2 mRNA containing the wild-type (or mutants) of the miR-19a-3p binding sequence was cloned into the downstream vector of the psicheck2-control luciferase reporter gene. e The interaction of YTHDF2 with miR-19a-3p was tested by luciferase reporter assay. Luciferase reporter gene assays was to measure the effect of miR-19a-3p on reporters, such as psicheck2-YTHDF2-wt and psicheck2-YTHDF2-mut in 293T cells. The experiment was repeated at least three times. The results are represented as the mean ± SD (n = 3). ns, no significance, **P < 0.01; ***P < 0.001

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