ArticleMolecular and cellular biochemistry2011
Lack of the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) is accompanied by increased CK2α' levels.
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 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Polymorphisms of DNA Repair Genes in Thyroid Cancer.International journal of molecular sciences · 2024Review
- Review
- The role of Ile3434Thr XRCC7 gene polymorphism in differentiated thyroid cancer risk in an Iranian population.Iranian biomedical journal · 2012Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-PKcs is the catalytic subunit of DNA-dependent protein kinase, an enzyme necessary for non-homologous end-joining (NHEJ) and hence repair of DNA double strand breaks. Characterization of two isogenic cell lines, M059K and M059J, which are DNA-PKcs-proficient and -deficient, respectively, revealed that lack of DNA-PKcs is accompanied by an increase in the protein level of one of the catalytic isozymes of protein kinase CK2, i.e., CK2α' and a concomitant increase in CK2 activity. The increase was also detectable at the mRNA level as measured by quantitative real time PCR. However, no increase at the DNA level was observed either by comparative PCR or fluorescent in situ hybridization indicating that gene amplification is not involved. Interestingly, only CK2α' was increased and not the other two subunits of CK2, i.e., CK2β or CK2α. In addition, the increase in CK2α' protein level was also observed in a DNA-PKcs-deficient mouse cell line.
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