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. 2019 Sep 26;20(5):4674–4682. doi: 10.3892/mmr.2019.10707

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Copyright: © Zou et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Blockade of SHH signaling in 16HBECs inhibits the HDM/TGF-β1-induced nuclear translocation of Gli1. The nuclear translocation of Gli1 was assessed by immunofluorescence staining. Cells were stained with an anti-Gli1 antibody (red) and DAPI (blue). Gli1 protein expression was increased in the treated cells compared to its expression in the control cells, and Gli1 was primarily localized to the nuclei of 16HBECs stimulated by HDM/TGF-β1 for 72 h. After the silencing of Gli1 using siRNA (A) or cyclopamine (B) the nuclear translocation of Gli1 was significantly decreased. A negative control siRNA (NC SiRNA) with no homology to known genes was used as a non-targeting control siRNA. Scale bar, 10 µm. SHH, Sonic hedgehog; HBECs, human bronchial epithelial cells; HDM, house dust mite; TGF-β1, transforming growth factor β1; Gli1, glioma-associated antigen-1; HBECs, human bronchial epithelial cells.