ArticleNucleic acids research2000
The C-terminal conserved domain of DNA-PKcs, missing in the SCID mouse, is required for kinase activity.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 65 citations in OpenAlex.
- Generation of NOD SCID mice with near-complete deletions of Il2rg and Prkdc for human cancer and HSC engraftment.Transgenic research · 2025Article
- Impaired synaptic transmission and long-term potentiation in severe combined immunodeficient (SCID) mice.Neuroreport · 2025Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- DNA-Dependent Protein Kinase Catalytic Subunit (DNA-PKcs): Beyond the DNA Double-Strand Break Repair.Molecules and cells · 2023Review
- FATC Domain Deletion Compromises ATM Protein Stability, Blocks Lymphocyte Development, and Promotes Lymphomagenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- DNA-PKcs promotes chromatin decondensation to facilitate initiation of the DNA damage response.Nucleic acids research · 2019Article
- "An End to a Means": How DNA-End Structure Shapes the Double-Strand Break Repair Process.Frontiers in molecular biosciences · 2019Review
- Molecular Evidence of Genome Editing in a Mouse Model of Immunodeficiency.Scientific reports · 2018Article
- DNA repair kinetics in SCID mice Sertoli cells and DNA-PKcs-deficient mouse embryonic fibroblasts.Chromosoma · 2017Article
- Non-redundant Functions of ATM and DNA-PKcs in Response to DNA Double-Strand Breaks.Cell reports · 2015Article
- Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining.Molecular cell · 2014Article
- The C-terminal residues of Saccharomyces cerevisiae Mec1 are required for its localization, stability, and function.G3 (Bethesda, Md.) · 2013Article
- DNA double strand break repair via non-homologous end-joining.Translational cancer research · 2013Article
- The N-terminal region of the DNA-dependent protein kinase catalytic subunit is required for its DNA double-stranded break-mediated activation.The Journal of biological chemistry · 2013Article
- Genetic evidence links the ASTRA protein chaperone component Tti2 to the SAGA transcription factor Tra1.Genetics · 2012Article
- Mutational analysis of the C-terminal FATC domain of Saccharomyces cerevisiae Tra1.Current genetics · 2010Article
- Tip60: connecting chromatin to DNA damage signaling.Cell cycle (Georgetown, Tex.) · 2010Review
- Non-homologous end joining in class switch recombination: the beginning of the end.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Activation Mechanism of Protein Kinase B by DNA-dependent Protein Kinase Involved in the DNA Repair System.Toxicological research · 2008Article
- p53 stabilization in response to DNA damage requires Akt/PKB and DNA-PK.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-PKcs, the catalytic subunit of DNA-dependent protein kinase (DNA-PK), has a phosphoinositol 3-kinase (PI 3-K) domain close to its C-terminus. Cell lines derived from the SCID mouse have been utilised as a model DNA-PKcs-defective system. The SCID mutation results in truncation of DNA-Pkcs at the extreme C-terminus leaving the PI 3-K domain intact. The mutated protein is expressed at low levels in most SCID cell lines, leaving open the question of whether the mutation abolishes kinase activity. Here, we show that a SCID cell line that expresses the mutant protein normally has dramatically impaired kinase activity. We estimate that the residual kinase activity typically present in SCID fibroblast cell lines is at least two orders of magnitude less than that found in control cells. Our results substantiate evidence that DNA-PKcs kinase activity is required for DSB rejoining and V(D)J recombination and show that the extreme C-terminal region of DNA-PKcs, present in PI 3-K-related protein kinases but absent in bona fide PI 3 lipid kinases, is required for DNA-PKcs to function as a protein kinase. We also show that expression of mutant DNA-PKcs protein confers a growth disadvantage, providing an explanation for the lack of DNA-PKcs expression in most SCID cell lines.
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