Keywordsprotein kinase CK2; metal toxicity; genome-wide screen; metal ion transport; zinc channels; therapeutic targets; pancreatic and duodenal homeobox protein PDX-1; PDX-1 C-terminus interacting factor PCIF1; protein kinase CK2; protein stability; CK2; Drosophila; Notch; eye development; neurogenesis; CK2; D11; HIF-1α; glioblastoma cells; gene expression profiling; autodisplay; human protein kinase CK2; non ATP-competitive inhibitor; peptide; CK2; neurodegeneration; synapse; signaling; CK2 inhibitors; GPCRs; CK2 substrates; CK2 knockout; CK2; cancer; indeno[1,2-b]indoles; pharmacophore; MOE; ZINC database; protein kinase CK2; casein kinase 2; ATP-competitive inhibitors; halogen bond; protein kinase CK2; skeletal muscle; C2C12; myopathy; protein kinase CK2; casein kinase 2; cancer; signal transduction; non oncogene addiction; phosphoproteomics; CRISPR/Cas9 technology; CK2; cancer; proliferation; apoptosis; migration; invasion; signaling pathways; signaling cascades; preclinical models; clinical trials; therapy; protein kinase CK2; subunit interface; cyclic peptides; protein–protein interaction; cell death; protein kinase CK2; protein kinase Rio1; phosphorylation; protein-protein interaction; benzimidazoles; adipogenesis; transcription factors; protein kinase; kinase inhibitor; Glioma; preclinical brain tumour; GBM therapeutic target; CK2 inhibitors; CX-4945; metronomic therapy; immune system; CK2; nanocapsules; nanoparticles; anti-CK2; RNAi; siRNA; tenfibgen; TBG; TBG-RNAi-CK2; therapy; cancer; targeting; cancer-specific; tumor-specific; prostate cancer; breast cancer; HNSCC; CK2; inhibitors; structure based drug design; ligand based drug design; cancer; hit optimization; protein kinase CK2; post-translational modification; regulatory networks; protein–protein interaction networks; hierarchical phosphorylation; post-translational modification interplay; n/a
