ArticleMolecular and cellular biology1996
Biochemical and genetic defects in the DNA-dependent protein kinase in murine scid lymphocytes.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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
56 citing papers in PubMed, 181 citations in OpenAlex.
- Article
- Review
- Diminished or inversed dose-rate effect on clonogenic ability in Ku-deficient rodent cells.Journal of radiation research · 2021Article
- DNA-dependent protein kinase in telomere maintenance and protection.Cellular & molecular biology letters · 2020Review
- Biological Characteristics of Severe Combined Immunodeficient Mice Produced by CRISPR/Cas9-MediatedFrontiers in genetics · 2019Article
- "An End to a Means": How DNA-End Structure Shapes the Double-Strand Break Repair Process.Frontiers in molecular biosciences · 2019Review
- Synergy between Prkdc and Trp53 regulates stem cell proliferation and GI-ARS after irradiation.Cell death and differentiation · 2017Article
- Review
- Dendritic cells induce Th2-mediated airway inflammatory responses to house dust mite via DNA-dependent protein kinase.Nature communications · 2015Article
- Functional intersection of ATM and DNA-dependent protein kinase catalytic subunit in coding end joining during V(D)J recombination.Molecular and cellular biology · 2013Article
- Lack of genomic instability in bone marrow cells of SCID mice exposed whole-body to low-dose radiation.International journal of environmental research and public health · 2013Article
- Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination.Cell cycle (Georgetown, Tex.) · 2011Review
- Article
- 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
- Fixing DNA breaks during class switch recombination.The Journal of experimental medicine · 2008Review
- DNA-PKcs and Artemis function in the end-joining phase of immunoglobulin heavy chain class switch recombination.The Journal of experimental medicine · 2008Article
- The catalytic subunit of DNA-protein kinase (DNA-PKcs) is not required for Ig class-switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- DNA-PKcs, but not TLR9, is required for activation of Akt by CpG-DNA.The EMBO journal · 2005Article
- p53-dependent and p53-independent pathways for radiation-induced immature thymocyte differentiation.Oncogene · 2004Article
- DNA-dependent protein kinase activity is not required for immunoglobulin class switching.The Journal of experimental medicine · 2002Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The scid gene product has been identified as the 460-kDa catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs p460), a member of the phosphatidylinositol 3-kinase family. DNA-PK activity is undetectable in scid cells, but the molecular basis for this defect has not been identified. Here we report that expression of p460 in scid lymphocyte precursors is detectable but is reduced at least 10-fold relative to that in wild-type lymphocytes. In addition, we show that the scid mutation disturbs p460 nuclear association, presumably affecting its role in DNA repair pathways. To examine the molecular basis for our observations, we used a degenerate PCR strategy to clone the C-terminal p460 kinase domain from wild-type and scid thymocytes. Northern (RNA) analysis with these probes revealed normal steady-state p460 mRNA levels in scid cells, suggesting that the reduced abundance of p460 protein is due to a posttranscriptional defect. Sequence comparisons identified a single-base-pair alteration in the scid C-terminal p460 kinase domain, resulting in a premature stop codon. This mutation is predicted to truncate p460 by approximately 8 kDa, but it preserves the conserved motifs required for kinase activity in members of the phosphoinositidyl 3-kinase family. Despite a computed molecular weight alteration of less than 2%, we were able to visualize this difference by Western blot (immunoblot) analysis of wild-type and scid p460. These data demonstrate that the scid DNA-PKes mutation is not a null allele and suggest a molecular rationale for the well-described leakiness of the scid phenotype.
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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.