ArticleMolecular and cellular biology2007
The E295K DNA polymerase beta gastric cancer-associated variant interferes with base excision repair and induces cellular transformation.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 94 citations in OpenAlex.
- DNA Polymerase Beta Catalytic and Fidelity Mutations Drive Platinum-Specific Drug Sensitivity.Cancers · 2026Article
- Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.International journal of radiation biology · 2026Review
- Harnessing DNA polymerase beta defect enhances synthetic lethality and treatment response in gastric cancer cells: implication for immunotherapy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2025Review
- SNP-Associated Substitutions of Amino Acid Residues in the dNTP Selection Subdomain Decrease Polβ Polymerase Activity.Biomolecules · 2024Article
- Unfilled gaps by polβ lead to aberrant ligation by LIG1 at the downstream steps of base excision repair pathway.Nucleic acids research · 2024Article
- Human Polβ Natural Polymorphic Variants G118V and R149I Affects Substate Binding and Catalysis.International journal of molecular sciences · 2023Article
- Interlocking activities of DNA polymerase β in the base excision repair pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- PA1 cells containing a truncated DNA polymerase β protein are more sensitive to gamma radiation.Radiation oncology journal · 2022Article
- The Role of Natural Polymorphic Variants of DNA Polymerase β in DNA Repair.International journal of molecular sciences · 2022Review
- Mouse Embryonic Fibroblasts Isolated From Nthl1 D227Y Knockin Mice Exhibit Defective DNA Repair and Increased Genome Instability.DNA repair · 2022Article
- L, D-Polydeoxyribonucleotides to provide an essential inhibitory effect on DNA polymerase β of human myeloid leukemia HL60 cells.Biochemistry and biophysics reports · 2020Article
- Article
- The Pol β variant containing exon α is deficient in DNA polymerase but has full dRP lyase activity.Scientific reports · 2019Article
- Detection of Somatic Mutation in Exon 12 of DNA Polymerase β in Ovarian Cancer Tissue SamplesIranian biomedical journal · 2018Article
- Crosstalk between mismatch repair and base excision repair in human gastric cancer.Oncotarget · 2017Article
- Mechanisms of DNA damage, repair, and mutagenesis.Environmental and molecular mutagenesis · 2017Review
- A Change in the Rate-Determining Step of Polymerization by the K289M DNA Polymerase β Cancer-Associated Variant.Biochemistry · 2017Article
- DNA Polymerase Beta Germline Variant Confers Cellular Response to Cisplatin Therapy.Molecular cancer research : MCR · 2017Article
- Base Excision Repair Variants in Cancer.Methods in enzymology · 2017Article
- The Tumor-Associated Variant RAD51 G151D Induces a Hyper-Recombination Phenotype.PLoS genetics · 2016Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Approximately 30% of human tumors examined for mutations in polymerase beta (pol beta) appear to express pol beta variant proteins (D. Starcevic, S. Dalal, and J. B. Sweasy, Cell Cycle 3:998-1001, 2004). Many of these variants result from a single amino acid substitution. We have previously shown that the K289M and I260M colon and prostate cancer variants, respectively, induce cellular transformation most likely due to sequence-specific mutator activity (S. Dalal et al., Biochemistry 44:15664-15673, 2005; T. Lang et al., Proc. Natl. Acad. Sci. USA 101:6074-6079, 2004; J. B. Sweasy et al., Proc. Natl. Acad. Sci. USA 102:14350-14355, 2005). In the work described here, we show that the E295K gastric carcinoma pol beta variant acts in a dominant-negative manner by interfering with base excision repair. This leads to an increase in sister chromatid exchanges. Expression of the E295K variant also induces cellular transformation. Our data suggest that unfilled gaps are channeled into a homology-directed repair pathway that could lead to genomic instability. The results indicate that base excision repair is critical for maintaining genome stability and could therefore be a tumor suppressor mechanism.
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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.