ArticleOncogene2002
Loss of heterozygosity and point mutation at Aprt locus in T cells and fibroblasts of Pms2-/- mice.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 24 citations in OpenAlex.
- Activation of FGFR2 Signaling Suppresses BRCA1 and Drives Triple-Negative Mammary Tumorigenesis That is Sensitive to Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Mutagenesis in vivo in T cells of p21-deficient mice.Mutation research · 2009Article
- Role of the mismatch repair gene, Msh6, in suppressing genome instability and radiation-induced mutations.Mutation research · 2008Article
- X-rays induce distinct patterns of somatic mutation in fetal versus adult hematopoietic cells.DNA repair · 2007Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mice null for the Pms2 mismatch repair (MMR) gene exhibit a predisposition to lymphoma, microsatellite repeat instability, and failure of spermatogenesis. To study the role of Pms2 in the maintenance of in vivo genomic integrity in somatic cells, we characterized Aprt mutations in T cells and fibroblasts of 129 x C3H Pms2-/-Aprt+/- mice. The spontaneous frequency of DAP-resistant T lymphocytes, as a consequence of APRT-deficiency, was increased threefold. Point mutation, which accounted for less than 20% of the DAP(r) mutant clones in Pms2+/+ mice, was predominant in the mutant T cell clones from Pms2-/- mice. These point mutations were predominantly TA to CG transitions. Fibroblasts of Pms2-/- mice exhibited only a modest increase in the frequency of clones with point mutations, such that mitotic recombination was still the primary cause of APRT deficiency. Thus, the mutator phenotype as a consequence of PMS2 deficiency is tissue-dependent, which may be related to the tissue-specific tumor proneness of Pms2-/- mice.
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Registered trials
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