ArticleMolecular and cellular biochemistry2005
Knocking out the regulatory beta subunit of protein kinase CK2 in mice: gene dosage effects in ES cells and embryos.
Article in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- CSNK2B-associated epilepsy: family report and literature review.Acta epileptologica · 2026Article
- CSNK2B Mutation: A Rare Cause of IGHD.Clinical endocrinology · 2025Article
- CK2β Regulates Hematopoietic Stem Cell Biology and Erythropoiesis.HemaSphere · 2023Article
- 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
- Splicing Interruption by Intron Variants inFrontiers in neuroscience · 2022Article
- Identification of de novo CSNK2A1 and CSNK2B variants in cases of global developmental delay with seizures.Journal of human genetics · 2019Article
- Protein kinase CK2 in development and differentiation.Biomedical reports · 2017Article
- The New Role for an Old Kinase: Protein Kinase CK2 Regulates Metal Ion Transport.Pharmaceuticals (Basel, Switzerland) · 2016Review
- Foxk1 recruits the Sds3 complex and represses gene expression in myogenic progenitors.The Biochemical journal · 2012Article
- CK2α is essential for embryonic morphogenesis.Molecular and cellular biochemistry · 2011Article
- Structure-function analysis of the beta regulatory subunit of protein kinase CK2 by targeting embryonic stem cell.Molecular and cellular biochemistry · 2011Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Knocking out the regulatory beta subunit of protein kinase CK2 in mice leads to early embryonic lethality. Heterozygous CK2beta (CK2beta+/-) knockout mice do not show an obvious phenotype. However, the number of heterozygous offsprings from CK2B+/- inter-crossings is lower than expected, meaning that some heterozygous embryos do not survive. Interestingly, CK2beta+/- ES (Embryonic Stem) cells express a considerably lower level of CK2beta than wild-type ES cells, whereas the level of CK2beta in organs from heterozygous adult mice does not significantly differ from those of wild-type mice. The data suggest a compensatory mechanism that adjusts CK2beta levels during development in the majority of, but not in all, cases (Mol Cell Biol 23: 908-915, 2003). In order to find an explanation for the gene dosage effect observed for heterozygous offsprings, we analysed embryos at mid-gestation (E10.5) as well as wild-type and CK2beta+/- ES cells for differences in growth rate and response to different stress agents. Analysis of E10.5 embryos generated from heterozygous matings revealed about 20% of smaller retarded CK2beta+/- embryos. No correlation between CK2beta levels in normal looking and retarded CK2beta+/- embryos were found. However, a different post-translational form of CK2beta protein has been detected in these retarded embryos. Cellular parameters such as growth rate and G1-, G2-checkpoints in ES cells were identical in both wild-type and CK2beta+/- cells. When ES cells were injected to induce differentiated teratocarcinoma in syngenic mice, the size of the tumours correlated with the level of CK2beta.
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Registered trials
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