Fig. 8
YTHDF2 binds to the m6A modification and stabilizes PELI2 mRNA. a RIP‒qPCR analysis revealed the enrichment of YTHDF1, YTHDF2, and YTHDF3 in the PELI2 transcript. The experiments were performed in quadruplicate, and the relative mRNA expression was compared to the input and is shown as the mean ± SD. One-way ANOVA, ****P < 0.0001. b Diagram showing the RNA probes used for RNA pull–down assays. c RNA pull–down of the endogenous YTHDF2 protein from cell extracts using PELI2 RNA probes with or without m6A modifications. Images are representative of three independent experiments. The full-length blots are presented in Additional file 8: Fig. S1. d, e PELI2 expression in ALKBH5- and YTHDF2-knockdown or control HaCaT cells was assessed by qRT‒PCR (d) and WB (e). The experiments were performed in triplicate. The relative mRNA expression level of PELI2 was quantified and is shown as the mean ± SD. One-way ANOVA, *P < 0.05, **P < 0.01. The full-length blots are presented in Additional file 8: Fig. S1. f ALKBH5- and YTHDF2-knockdown or control HaCaT cells were treated with actinomycin D (5 μg/mL) for 0, 2, 4, 6, and 8 h. The mRNA expression of PELI2 was analyzed by qRT–PCR. The experiments were performed in triplicate. g Schematic diagram showing how the reduction in m6A methylation mediated by the upregulation of the m6A eraser protein ALKBH5 facilitates wound re-epithelialization by enhancing PELI2 mRNA stability in a YTHDF2-dependent manner