ArticleMolecular and cellular biology2014
Identification of a novel protein interaction motif in the regulatory subunit of casein kinase 2.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Structural basis for TRF2-RAP1 recruitment by EBNA1 at the EBV origin of replication.Scientific reports · 2026Article
- Structural Basis for TRF2-RAP1 Recruitment by EBNA1 at the EBV origin of replication.Research square · 2025Article
- Reply to van Schie et al.: ARK2N in TCR: Across in vivo and in vitro studies.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Evidence that ARK2N is not a core factor in transcription-coupled DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A CK2 and SUMO-dependent, PML NB-involved regulatory mechanism controlling BLM ubiquitination and G-quadruplex resolution.Nature communications · 2023Article
- Changes in SUMO-modified proteins in Epstein-Barr virus infection identifies reciprocal regulation of TRIM24/28/33 complexes and the lytic switch BZLF1.PLoS pathogens · 2023Article
- Protein Kinase CK2 and Epstein-Barr Virus.Biomedicines · 2023Review
- Functional diversity: update of the posttranslational modification of Epstein-Barr virus coding proteins.Cellular and molecular life sciences : CMLS · 2022Review
- Placental Mammals Acquired Functional Sequences in NRK for Regulating the CK2-PTEN-AKT Pathway and Placental Cell Proliferation.Molecular biology and evolution · 2022Article
- Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function.PLoS pathogens · 2022Article
- Comparing Two Neurodevelopmental Disorders Linked to CK2: Okur-Chung Neurodevelopmental Syndrome and Poirier-Bienvenu Neurodevelopmental Syndrome-Two Sides of the Same Coin?Frontiers in molecular biosciences · 2022Review
- The Epstein-Barr Virus BMRF1 Protein Activates Transcription and Inhibits the DNA Damage Response by Binding NuRD.Journal of virology · 2019Article
- Identification of ARKL1 as a Negative Regulator of Epstein-Barr Virus Reactivation.Journal of virology · 2019Article
- A Screen for Epstein-Barr Virus Proteins That Inhibit the DNA Damage Response Reveals a Novel Histone Binding Protein.Journal of virology · 2018Article
- EBNA1-targeted inhibitors: Novel approaches for the treatment of Epstein-Barr virus-associated cancers.Theranostics · 2018Review
- Co-Localization of Insulin-Like Growth Factor Binding Protein-1, Casein Kinase-2β, and Mechanistic Target of Rapamycin in Human Hepatocellular Carcinoma Cells as Demonstrated by Dual Immunofluorescence and in Situ Proximity Ligation Assay.The American journal of pathology · 2018Article
- ERK2 phosphorylation of EBNA1 serine 383 residue is important for EBNA1-dependent transactivation.Oncotarget · 2016Article
- Modular transcriptional repertoire and MicroRNA target analyses characterize genomic dysregulation in the thymus of Down syndrome infants.Oncotarget · 2016Article
- The intracellular domain of teneurin-1 induces the activity of microphthalmia-associated transcription factor (MITF) by binding to transcriptional repressor HINT1.The Journal of biological chemistry · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Casein kinase 2 (CK2) regulates multiple cellular processes and can promote oncogenesis. Interactions with the CK2β regulatory subunit of the enzyme target its catalytic subunit (CK2α or CK2α') to specific substrates; however, little is known about the mechanisms by which these interactions occur. We previously showed that by binding CK2β, the Epstein-Barr virus (EBV) EBNA1 protein recruits CK2 to promyelocytic leukemia (PML) nuclear bodies, where increased CK2-mediated phosphorylation of PML proteins triggers their degradation. Here we have identified a KSSR motif near the dimerization interface of CK2β as forming part of a protein interaction pocket that mediates interaction with EBNA1. We show that the EBNA1-CK2β interaction is primed by phosphorylation of EBNA1 on S393 (within a polyserine region). This phosphoserine is critical for EBNA1-induced PML degradation but does not affect EBNA1 functions in EBV replication or segregation. Using comparative proteomics of wild-type (WT) and KSSR mutant CK2β, we identified an uncharacterized cellular protein, C18orf25/ARKL1, that also binds CK2β through the KSSR motif and show that this involves a polyserine sequence resembling the CK2β binding sequence in EBNA1. Therefore, we have identified a new mechanism of CK2 interaction used by viral and cellular proteins.
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