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Interestingly, the DNA damage repair protein RRM2, often upregulated in NB to support oncogenicity, was upregulated across all conditions, and phosphorylation at the Ser-80 and Ser-86 sites was significantly downregulated by both combinations ( Supplementary Table S1 ) ( Based on the phosphoproteomic profiling we then inferred the upstream kinases responsible for the differential phosphorylation observed in each treatment versus control, using a kinase enrichment analysis ( Figure 6 )
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