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. 2020 Apr 4;12(4):878. doi: 10.3390/cancers12040878

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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CHK1 expression, activation by rucaparib, and inhibition by PF-477736 in BRCA2 mutant and corrected cells. Cells were exposed for 24 h to DMSO, rucaparib, or rucaparib and PF-477736 and analysed for pCHK^S345, CHK1, and pCDK1^Tyr15. Vinculin was used as a loading control for pCHK^S345, CHK1, pCDK1^Tyr15 and CDK1, and GAPDH was used as the loading control for CHK1^S296 (a) Western blot from a single representative experiment. (b) Densitometry was calculated using Syngene software of CHK1 expression normalised to Vinculin. (c) Normalised densitometry of phosphorylated CHK1 and CDK1. Data are the mean and standard deviation of three individual experiment.