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. 2015 Apr 29;10(5):373–383. doi: 10.1080/15592294.2015.1028708

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Marcella Salzano, Marta Sanz-García, Diana M Monsalve, David S Moura, and Pedro A Lazo

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 6. — VRK1 activity is required for γH2AX foci formation. (A) Active VRK1 resistant to siRNA rescues formation of γH2AX foci. Endogenous VRK1 in A549 cells was knocked-down with siVRK1-01 followed 2 d later by transfection with a plasmid expressing HA-VRK1-R (with 3 substitutions that make it resistant only to si-VRK1-01)¹⁸ (VRK1-R in the figure) or its kinase-dead form (VRK1-R-K_D in the figure). Cells were analyzed by immunofluorescence confocal microscopy. The number of foci in cells was counted and significance determined using ANOVA analysis. (B) Effect of inhibitors KU55933 and caffeine on γH2AX foci formation. A549 cells were treated with si-Control or si-VRK1-02 and the effect of KU55933 and caffeine on γH2AX foci induced by IR determined. The number of γH2AX foci was quantified.