ArticleMolecular and cellular biochemistry2011
Protein kinase CK2 accumulation in "oncophilic" cells: causes and effects.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Deciphering O‑GlcNAc-Dependent Signaling Via Integrated Proteomics and Phosphoproteomics.ACS omega · 2026Article
- CK2 in the spotlight: decoding its role in hematological malignancies and therapeutic applications.Discover oncology · 2025Review
- Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024Review
- Discovery of a CK2α'-Biased ATP-Competitive Inhibitor from a High-Throughput Screen of an Allosteric-Inhibitor-Like Compound Library.ACS chemical neuroscience · 2024Article
- Identification of CK2α' selective inhibitors by the screening of an allosteric-kinase-inhibitor-like compound library.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic targeting of CK2 in acute and chronic leukemias.Leukemia · 2018Review
- Exploring the CK2 Paradox: Restless, Dangerous, Dispensable.Pharmaceuticals (Basel, Switzerland) · 2017Review
- Structural Hypervariability of the Two Human Protein Kinase CK2 Catalytic Subunit Paralogs Revealed by Complex Structures with a Flavonol- and a Thieno[2,3-d]pyrimidine-Based Inhibitor.Pharmaceuticals (Basel, Switzerland) · 2017Article
- Review
- Synthesis and properties of a selective inhibitor of homeodomain-interacting protein kinase 2 (HIPK2).PloS one · 2014Article
- Co-expressions of casein kinase 2 (CK2) subunits restore the down-regulation of tubulin levels and disruption of microtubule structures caused by PrP mutants.Journal of molecular neuroscience : MN · 2013Article
- Protein kinase CK2 in hematologic malignancies: reliance on a pivotal cell survival regulator by oncogenic signaling pathways.Leukemia · 2012Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At variance with protein kinases expressed by oncogenes, CK2 is endowed with constitutive activity under normal conditions, and no CK2 gain-of-function mutants are known. Its amount, however, is abnormally high in malignant cells where it appears to be implicated in many of the cell biology phenomena associated with cancer. These observations can be reconciled assuming that tumor cells develop an overdue reliance ("non-oncogene addiction") on abnormally high CK2 level. While the potential of this latter to generate an environment favorable to neoplasia is consistent with the global antiapoptotic and prosurvival role played by CK2, it is not clear what is determining accumulation of CK2 in cells "predisposed" to become malignant. Exploiting the apoptosis sensitive (S) or resistant (R) CEM cell model, characterized by sharply different CK2 levels, we have now correlated the level and degradation rate of CK2 to those of the chaperone proteins Hsp90 and Cdc37. We show in particular that persistence of high CK2 level in R-CEM, as opposed to S-CEM, is accompanied by the presence of an immunospecific form of Cdc37 not detectable in S-CEM and refractory to staurosporine-induced degradation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.