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. 2021 Apr 12;28(9):2690–2707. doi: 10.1038/s41418-021-00778-z

Fig. 4. USP24-stabilized E2F4 represses Rad51 transcriptional activity.

Fig. 4

The protein (A) and mRNA (B) levels of Rad51 in A549 cells with or without USP24 knockdown were studied by Western blot and RT-PCR assays. The luciferase activity driven by the promoter of rad51 with or without deletion or mutation of the E2F-binding site was studied (C). The mRNA level of Rad51 (D) and luciferase activity driven by promoter of rad51 (E) with or without USP24 in the absence or presence of E2F4 overexpression was studied. The recruitment of E2F4 to the promoter of rad51 in A549 cells in the absence or presence of USP24 was studied by ChIP assay (F). The cell viability and DDR activity of A549 cells with or without CPT treatment and USP24 knockdown were studied by flow cytometry (G) and Rad51 foci assays (H). The distribution of Rad51 colocalized with chromatin in cells with or without USP24 knockdown under CPT treatment was studied by Western blotting analysis with the indicated antibodies (I). The results from three independent experiments were statistically analyzed using a t-test: *p < 0.05, **p < 0.01, ***p < 0.005.