ArticleCancer science2005
Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice.
Article in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 51 citations in OpenAlex.
- Cross-tissue transcriptome-wide association studies identify genetic susceptibility genes for prostate cancer.BMC cancer · 2025Article
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- Manganese Is a Strong Specific Activator of the RNA Synthetic Activity of Human Polη.International journal of molecular sciences · 2021Article
- Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021Review
- Review
- Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?PLoS genetics · 2017Review
- Mouse DNA polymerase ι lacking the forty-two amino acids encoded by exon-2 is catalytically inactive in vitro.DNA repair · 2017Article
- DNA polymerase iota (Pol ι) promotes invasion and metastasis of esophageal squamous cell carcinoma.Oncotarget · 2016Article
- The Regulation of DNA Damage Tolerance by Ubiquitin and Ubiquitin-Like Modifiers.Frontiers in genetics · 2016Review
- 129-Derived Mouse Strains Express an Unstable but Catalytically Active DNA Polymerase Iota Variant.Molecular and cellular biology · 2015Article
- The error-prone DNA polymerase ι provides quantitative resistance to lung tumorigenesis and mutagenesis in mice.Oncogene · 2014Article
- Mcm10 deficiency causes defective-replisome-induced mutagenesis and a dependency on error-free postreplicative repair.Cell cycle (Georgetown, Tex.) · 2014Article
- Biological and therapeutic relevance of nonreplicative DNA polymerases to cancer.Antioxidants & redox signaling · 2013Review
- Translesion DNA synthesis and mutagenesis in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- Modulation of mutagenesis in eukaryotes by DNA replication fork dynamics and quality of nucleotide pools.Environmental and molecular mutagenesis · 2012Review
- Translesion DNA synthesis in the context of cancer research.Cancer cell international · 2011Article
- Inaccurate DNA synthesis in cell extracts of yeast producing active human DNA polymerase iota.PloS one · 2011Article
- Translesion synthesis polymerases in the prevention and promotion of carcinogenesis.Journal of nucleic acids · 2010Article
- Influence of local sequence context on damaged base conformation in human DNA polymerase iota: molecular dynamics studies of nucleotide incorporation opposite a benzo[a]pyrene-derived adenine lesion.Nucleic acids research · 2009Article
- Y-family DNA polymerases in mammalian cells.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pol iota is a member of the Y-family DNA polymerases, characterized by their capacity for translesion DNA synthesis and low fidelity base incorporation, and has therefore been assumed to play important roles in mutagenesis and carcinogenesis. In fact, the mouse Pol iota gene is located within the Par2 (pulmonary adenoma resistance 2) locus on distal chromosome 18, which we have identified as a major susceptibility locus regarding urethane induction of pulmonary adenomas. Indeed, Pol iota has been suggested to be a candidate for Par2 from both the genetic and biological standpoints. Taking advantage of 129X1/SvJ mice naturally deficient in Pol iota due to a nonsense mutation within the coding region of the gene, we here analyzed urethane-treated (A/J x 129X1/SvJ)F(1) x A/J backcross and (A/J x 129X1/SvJ)F(2) intercross mice and observed the defective 129X1/SvJ Pol iota allele to be genetically linked with an increased susceptibility to lung tumors relative to the A/J allele. Thus, among the already known mouse Pol iota alleles, the defective 129X1/SvJ allele is associated exclusively with the highest susceptibility to lung tumors. The result indicates a possibility that the Pol iota gene may participate in error-free repair of damaged DNA and prevention of lung tumor development.
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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.