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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Oncogene. 2021 Jun 22;40(30):4872–4883. doi: 10.1038/s41388-021-01881-8

Figure 6. Overexpression of Cyclin D1 rescues both the E2F1 protein expression and the CDK4/6 kinase activity defects caused by PARP14 knockdown.

Figure 6.

A. Cell cycle profiles of RPE-1 WT and cyclin D1-overexpressing cells upon PARP14 knockdown. B. Quantification showing the percent of RPE-1 WT and cyclin D1-overexpressing cells in G1 cell cycle phase upon PARP14 knockdown. Bars represent the means ± SEM (t-test, unpaired). C. Cell cycle profiles of RPE-1 WT and cyclin D1-overexpressing cells upon PARP14 knockdown and subsequent treatment with 200ng/mL nocodazole for 24h. D. Quantification showing the percent of RPE-1 WT and cyclin D1-overexpressing cells in G2/M cell cycle phase upon PARP14 knockdown and subsequent treatment with 200ng/mL nocodazole for 24h. Bars represent the means ± SEM (t-test, unpaired). E. Western blots showing the levels of phosphorylated RB at Ser780, E2F1 and Cdc6 upon PARP14 knockdown in RPE-1 WT or cyclin D1- overexpressing cells. To facilitate direct comparison, longer film exposures are shown for the RPE-1 WT samples and shorter film exposures are shown for the RPE-1 cyclin D1-overexpressing samples. F. In vitro kinase assay using recombinant RB as a substrate and Cyclin D1/CDK4 kinase complexes immunoprecipitated from RPE-1 WT or cyclin D1- overexpressing cells upon PARP14 knockdown. To facilitate direct comparison, longer film exposures are shown for the RPE-1 WT samples and shorter film exposures are shown for the RPE-1 cyclin D1-overexpressing samples.