Protein kinase CK2 is required for the recruitment of 53BP1 to sites of DNA double-strand break induced by radiomimetic drugs

Cancer Letters
Barbara GuerraOlaf-Georg Issinger

Abstract

The ataxia telangiectasia mutated (ATM) signaling pathway responds rapidly to DNA double-strand breaks (DSBs) and it is characterized by recruitment of sensor, mediator, transducer and repair proteins to sites of DNA damage. Data suggest that CK2 is implicated in the early cellular response to DSBs. We demonstrate that CK2 binds constitutively the adaptor protein 53BP1 through the tandem Tudor domains and that the interaction is disrupted upon induction of DNA damage. Down-regulation of CK2 results in significant reduction of (i) 53BP1 foci formation, (ii) binding to dimethylated histone H4 and (iii) ATM autophosphorylation. Our data suggest that CK2 is required for 53BP1 accumulation at sites of DSBs which is a prerequisite for efficient activation of the ATM-mediated signaling pathway.

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Apr 5, 2016·Oncogene·E MandatoF Piazza
May 21, 2015·Cellular and Molecular Life Sciences : CMLS·Odile FilholClaude Cochet
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Jul 11, 2018·Proceedings of the National Academy of Sciences of the United States of America·Laura E BowieRay Truant
Jun 10, 2017·Molecular and Cellular Biochemistry·Susanne Schaefer, Barbara Guerra
May 1, 2021·International Journal of Molecular Sciences·Zaira SpinelloSabrina Manni

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