Murine Prkdc polymorphisms impact DNA-PKcs function
Open accessAbstract
Polymorphic variants of DNA repair genes can increase the carcinogenic potential of exposure to ionizing radiation. Two single nucleotide polymorphisms (SNPs) in Prkdc, the gene encoding the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), have been identified in BALB/c mice and linked to reduced DNA-PKcs activity and mammary cancer susceptibility. We examined three additional mouse strains to better define the roles of the BALB/c Prkdc SNPs (R2140C and M3844V). One is a congenic strain (C.B6) that has the C57BL/6 Prkdc allele on a BALB/c background, and the other is a congenic strain (B6.C) that has the BALB/c variant Prkdc allele on a C57BL/6 background. We also examined the LEWES mouse strain, which possesses only one of the BALB/c Prkdc SNPs (M3844V). Our results demonstrate that both Prkdc SNPs are responsible for deficient DNA-PKcs protein expression, DNA repair and telomere function, while the LEWES SNP affects only DNA-PKcs expression and repair capacity. These studies provide insight into the separation of function between the two BALB/c SNPs as well as direct evidence that SNPs positioned within Prkdc can significantly influence DNA-PKcs function involving DNA repair capacity, telomere end-capping, and potentially cancer susceptibility.
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Balb/c mice have 2 different polymorphisms in DNA-dependent protein kinase (DNA-PKcs) that mediates non-homologous end joining, which results in decreased but not absent function.
“Balb/c mice have 2 different polymorphisms in DNA-dependent protein kinase (DNA-PKcs) that mediates non-homologous end joining, which results in decreased but not absent function [42], [43], [44].”
From Hindlimb suspension and spe-like radiation impairs clearance of bacterial infections (2014) · cites this paper as [42]
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References 31 · Cited by 13
- Authors
- Fabre, K. M., Ramaiah, L., Dregalla, R. C., Desaintes, C., Weil, M. M., Bailey, S. M., & Ullrich, R. L.
- Affiliations
- Colorado State University (US)
- Huntingdon Life Sciences, East Millstone, New Jersey 08875-2360
- European Commission (BE)
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Ullrich, Robert L
- Venue
- Radiation Research
- Publisher
- Radiation Research Society
- Published
- 2011-01-25
- Volume
- 175
- Issue
- 4
- Pages
- 493
- ISSN
- 0033-7587 (ISSN-L)
- PMC
- PMC3102216
- OpenAlex
- W2067866257
- Cited by
- 13
- References
- 31
- Citations by year
- 2025: 1 · 2021: 1 · 2020: 1 · 2018: 2 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 1
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Radiation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- BioOne Complete (BioOne) (submittedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (T32CA009236, R01CA043322, CA043322, CA 09236)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- PRKDC, DNA-PKcs, single nucleotide polymorphisms, DNA repair, ionizing radiation carcinogenesis, congenic mice, BALB/c mice, C57BL/6 mice, protein expression
- MeSH terms
- Animals, DNA, DNA Repair, DNA-Binding Proteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nuclear Proteins, Species Specificity, Polymorphism, Single Nucleotide, Mice, DNA-Activated Protein Kinase
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