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Fig. 7 | Stem Cell Research & Therapy

Fig. 7

From: miR-106b regulates the proliferation and differentiation of neural stem/progenitor cells through Tp53inp1-Tp53-Cdkn1a axis

Fig. 7

miR-106b inhibits the differentiation of NPCs through Tp53inp1-Tp53-Cdkn1a axis. a A schematic representation of the experimental approach. b qPCR analysis of levels of miR-106b and transcripts corresponding to Tp53inp1 and Cdkn1a in all experimental groups versus controls. c qPCR analysis of levels of transcripts corresponding to Ki67, Tuj1, and GFAP in all experimental groups versus controls. d Immunofluorescence analysis of transduced cells displaying Ki67/Nestin and Tuj1/GFAP immunoreactivities in all experimental groups versus controls. e Quantification of cells expressing Ki67/Nestin and Tuj1/GFAP immunoreactivities in all experimental groups versus controls. f A schematic representation of miR-106b-mediated regulation of NPCs to facilitate proliferation: Tp53inp1-Tp53-Cdkn1a axis is a key inducer for cell cycle exit and differentiation of NPCs. The high levels of miR-106b inhibit Tp53inp1 and Cdkn1a expression, which maintains the proliferation of NPCs. The downregulation of miR-106b expression activates Tp53inp1-Tp53-Cdkn1a axis, leading to the decline of NPCs pool and the generation of both neurons and glia. Scale bar, 20 μm (d). Data are mean ± SD. ∗∗∗∗p < 0.0001, ∗∗∗p < 0.001, ∗∗p < 0.01, and ∗p < 0.05. ####p < 0.0001, ###p < 0.001, ##p < 0.01, and #p < 0.05 versus the miR-106b LOF groups. Experiments were carried out three times in triplicates for in vitro perturbation

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