DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169.

Consistent with our findings that RNF169 was able to inhibit 53BP1 IRIF formation when DYRK1A was inhibited by harmine ( Figure 3 ), we observed that overexpression of GFP-RNF169 in the DYRK1A-KO U-2 OS cells also results in inhibition of the 53BP1 recruitment to DSBs ( Figure 6(a , b ), the differences between the GFP- and GFP-RNF169-expressing cells were highly significant in all cell lines, p < 0.001).

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A similar trend was also observed in the second U-2 OS DYRK1A-KO clone although the differences with the parental control did not reach statistical significance due to high experimental variability.

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