Bioinformatic Investigation of Regulatory Elements in the Core Promoters of CK2 Genes and Pseudogene
Protein kinase CK2 is an important regulator of cell, embryo, and organism function whose transcript levels are often dysregulated in disease. Previous studies have primarily focused on the regulation of CK2 gene expression via the proximal promoter. Here, we analyzed the core promoter of the CK2 genes and pseudogene to assess the structure and potential regulatory elements. Our analysis showed that CSNK2A1 contained 14 exons, rather than 13 exons as previously reported. Using FANTOM5 and DBTTS data, we found that transcription start sites were broadly distributed across a 100-nucleotide region in the CK2 gene core promoters, consistent with “broad” class promoter architecture. Using these databases, we found a dissimilar transcription start site usage between adult and cancer tissues compared to fetal tissues for each of the CK2 gene promoters. A further analysis of the CK2 gene core promoter subregions showed instances of core promoter subregion switching. All CK2 gene core promoters contained canonical and non-canonical initiator motifs, suggesting their potential as dual-initiator core promoters, while CSNK2A3 only had canonical initiator motifs. Additionally, all CK2 gene core promoters contain DCE motifs and pause buttons. In contrast, Wnt/β-catenin target genes c-MYC and CCND1 had DPEs, which can be regulated by protein kinase CK2. Collectively, our data provides new insights into the transcriptional regulation of CK2 genes and opens new avenues for research.
Authors
- Nicholas G. Wilson (ORCID: https://orcid.org/0000-0001-5158-2539)
- Jesse S. Basra (ORCID: https://orcid.org/0000-0003-4925-2543)
- Isabel Domínguez (ORCID: https://orcid.org/0009-0002-6000-0734)
Institutions
- Boston University (US)
- Georgetown University (US)
Publication Details
- Journal
- Kinases and Phosphatases
- Published
- 2025-11-04
- DOI
- https://doi.org/10.3390/kinasesphosphatases3040022
- Primary Topic
- Protein Kinase Regulation and GTPase Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00