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Protein kinase CK2 is involved in several cellular processes and has latelyalso been linked to the DNA damage response through phosphorylations and interactions.Herein, we have analysed two sets of mouse cell lines, one pair, which is proficientand deficient in ATM and the other set expressing or lacking a functional catalyticsubunit of the DNA dependent protein kinase (DNA-PKcs). Both kinases are implicatedin the downstream phosphorylation of the signaling molecules such as BID and AKT1in response to DNA damage. BID and AKT1 are also targets of CK2, hence the fourcell lines were treated with the three established CK2 inhibitors DMAT, TBB andresorufin in the absence and presence of the radiomimetic drug neocarzinostatin,which induces DNA double-strand breaks. We show that there are differences withrespect to the effect of the CK2 inhibitors on the phosphorylation of AKT1 atS473 and its downstream target GSK3β as well as between the two sets of cell lines.However, no such change was seen with BID phosphorylation. The most notably differencewas the higher expression of CK2α' and CK2β in DNA-PKcs defective cells comparedto the DNA-PKcs proficient cells.

Characterization of ATM and DNA-PK wild-type and mutant cell lines upon DSB induction in the presence and absence of CK2 inhibitors