Fig. 2: HMGA1 increased the expression of MYH9 through c-Jun-mediated transcription. | Cell Death & Disease

Fig. 2: HMGA1 increased the expression of MYH9 through c-Jun-mediated transcription.

From: HMGA1 stimulates MYH9-dependent ubiquitination of GSK-3β via PI3K/Akt/c-Jun signaling to promote malignant progression and chemoresistance in gliomas

Fig. 2

A Knockdown HMGA1 leads to the decreasing of MYH9 mRNA expression. B Schematic diagram of putative c-Jun binding sites in MYH9 promotor and the primers of each binding site. C, D Knockdown c-Jun induced inhibition of MYH9 mRNA (C) and protein (D) expression. E c-Jun bound to all the predicted sites inside the transcription regulatory region of MYH9, and knockdown of c-Jun could inhibit the protein–DNA interactions in all three binding sites. F Dual-luciferase reporter assay showed that the reporter plasmid with the promotor region of MYH9 resulted in a significant decrease in luciferase activity after transfection with si-c-Jun, whereas the plasmid without MYH9 promotor had no change in luciferase activity.

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