Protein kinase CK2 is required for the recruitment of 53BP1 to sites of DNA double-strand break induced by radiomimetic drugs》.pdf
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Protein kinase CK2 is required for the recruitment of 53BP1 to sites of DNA double-strand break induced by radiomimetic drugs》.pdf
Cancer Letters 345 (2014) 115–123
Contents lists available at ScienceDirect
Cancer Letters
journal homepage: www.else /locate/canlet
Protein kinase CK2 is required for the recruitment of 53BP1 to sites
of DNA double-strand break induced by radiomimetic drugs
Barbara Guerra a,⇑, Kuniyoshi Iwabuchi b, Olaf-Georg Issinger a
a Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark
b Department of Biochemistry, Kanazawa Medical University, Ishikawa, Japan
a r t i c l e i n f o a b s t r a c t
Article history: The ataxia telangiectasia mutated (ATM) signaling pathway responds rapidly to DNA double-strand
Received 20 October 2013 breaks (DSBs) and it is characterized by recruitment of sensor, mediator, transducer and repair proteins
Received in revised form 26 November 2013 to sites of DNA damage. Data suggest that CK2 is implicated in the early cellular response to DSBs. We
Accepted 29 November 2013
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
Keywords:
autophosphorylation. Our data suggest that CK2 is required for 53BP1 accumulation at sites of DSBs
CK2
53BP1
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