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Fig. 5 | Inflammation and Regeneration

Fig. 5

From: ALKBH5-mediated m6A demethylation fuels cutaneous wound re-epithelialization by enhancing PELI2 mRNA stability

Fig. 5

ALKBH5 expression is positively correlated with PELI2 expression levels. a IGV tracks of PELI2 expression according to the RNA-seq analysis of ALKBH5-knockdown or control HaCaT cells. The experiments were performed in duplicate. b PELI2 protein expression was measured in HaCaT cells after ALKBH5 knockdown by WB. The full-length blots are presented in Additional file 8: Fig. S1. c PELI2 expression in the skin at the wound edge of WT and Alkbh5‒/‒ mice was visualized by IF staining at PWD8. Dotted lines denote epidermal boundaries. Scale bar: 100 μm. d qRT-PCR showed the mRNA expression of PELI2 in primary keratinocytes derived from WT and Alkbh5‒/‒ mice. The experiments were performed in triplicate, and the relative mRNA expression is shown as the mean ± SD. t test, two-sided **P < 0.01. e The expression and colocalization of PELI2 and ALKBH5 in the epidermis at the wound edge of WT mice were visualized using IF staining at PWD6. Scale bar: 100 μm. f IGV tracks displaying the MeRIP-seq read coverage of PELI2 after ALKBH5 knockdown. The experiments were performed in duplicate. g Increased m6A modification in PELI2 transcripts after ALKBH5 knockdown in HACAT cells, as assessed by gene-specific m6A-RIP-qPCR assays. The experiments were performed in triplicate, and the relative expression of mRNA in each group was compared to the input and is shown as the mean ± SD. One-way ANOVA, ns not significant, *P < 0.05, ****P < 0.0001

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