YTHDF1 deficiency aggravates hepatic inflammatory response via ERK and NF-κB pathway. (IMAGE)
Caption
(A–C) Serum samples collected at 0 h, 3 h, 8 h, and 24 h after ConA (8 mg/kg) injection from Fig. 2B and C was measured for IL-6 (A), CXCL1 (B), and TNF-α (C) levels, n = 3–5 per group. (D) Liver tissues of Ythdf1−/− (KO) and WT mice collected at 8 h after ConA (8 mg/kg) treatment were extracted for RNA, followed by RNA-Seq analysis, n = 3–4 per group. GSEA analysis for RNA-Seq data identified the significant up-regulation or down-regulation gene sets of hallmarks mediated by YTHDF1 deletion upon ConA challenge for 8 h. (E) Representative hallmark pathways were shown for GSEA analysis. (F, G) Liver tissues harvested at 0 h, 3 h, and 8 h after ConA (8 mg/kg) treatment were immunoblot analyzed for the inflammatory pathway (F), followed by gray analysis using image J (G). (H) GSEA analysis of GOBP gene sets showed over-activation of ERK and NF-κB pathway mediated by YTHDF1 deletion upon ConA (8 mg/kg) challenge for 8 h. Data are presented as mean ± SD; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 compared with two groups of the corresponding time-point, based on unpaired two-sided Student's t-test. NES, normalized enrichment score. FRD, false discovery rate. KO, Ythdf1−/−.
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Genes & Diseases
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