ArticleThe Journal of biological chemistry2012
Colon cancer-associated DNA polymerase β variant induces genomic instability and cellular transformation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 43 citations in OpenAlex.
- The S180R Human Germline Variant of DNA Polymerase β Is a Low Fidelity Enzyme with Reduced Flexibility of the Fingers Domain.Biochemistry · 2026Article
- DNA polymerase beta expression in head & neck cancer modulates the poly(ADP-ribose)-mediated replication checkpoint.DNA repair · 2025Article
- 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
- Unfilled gaps by polβ lead to aberrant ligation by LIG1 at the downstream steps of base excision repair pathway.Nucleic acids research · 2024Article
- Mouse models to explore the biological and organismic role of DNA polymerase beta.Environmental and molecular mutagenesis · 2024Review
- The Role of Natural Polymorphic Variants of DNA Polymerase β in DNA Repair.International journal of molecular sciences · 2022Review
- Two polymorphic mutations in promoter region of DNA polymerase β in relatively higher percentage of thymic hyperplasia patients.Thoracic cancer · 2021Article
- Mutation in DNA Polymerase Beta Causes Spontaneous Chromosomal Instability and Inflammation-Associated Carcinogenesis in Mice.Cancers · 2019Article
- The Pol β variant containing exon α is deficient in DNA polymerase but has full dRP lyase activity.Scientific reports · 2019Article
- Single molecule glycosylase studies with engineered 8-oxoguanine DNA damage sites show functional defects of a MUTYH polyposis variant.Nucleic acids research · 2019Article
- DNA Polymerase β Cancer-Associated Variant I260M Exhibits Nonspecific Selectivity toward the β-γ Bridging Group of the Incoming dNTP.Biochemistry · 2017Article
- Remote Mutations Induce Functional Changes in Active Site Residues of Human DNA Polymerase β.Biochemistry · 2017Article
- A Change in the Rate-Determining Step of Polymerization by the K289M DNA Polymerase β Cancer-Associated Variant.Biochemistry · 2017Article
- Regulation of DNA Alkylation Damage Repair: Lessons and Therapeutic Opportunities.Trends in biochemical sciences · 2017Review
- Base excision repair of oxidative DNA damage: from mechanism to disease.Frontiers in bioscience (Landmark edition) · 2017Review
- 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
- R152C DNA Pol β mutation impairs base excision repair and induces cellular transformation.Oncotarget · 2016Article
- Gut Microbiota Imbalance and Base Excision Repair Dynamics in Colon Cancer.Journal of Cancer · 2016Review
- The K167I variant of DNA polymerase β that is found in Esophageal Carcinoma patients impairs polymerase activity and BER.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Rapidly advancing technology has resulted in the generation of the genomic sequences of several human tumors. We have identified several mutations of the DNA polymerase β (pol β) gene in human colorectal cancer. We have demonstrated that the expression of the pol β G231D variant increased chromosomal aberrations and induced cellular transformation. The transformed phenotype persisted in the cells even once the expression of G231D was extinguished, suggesting that it resulted as a consequence of genomic instability. Biochemical analysis revealed that its catalytic rate was 140-fold slower than WT pol β, and this was a result of the decreased binding affinity of nucleotides by G231D. Residue 231 of pol β lies in close proximity to the template strand of the DNA. Molecular modeling demonstrated that the change from a small and nonpolar glycine to a negatively charged aspartate resulted in a repulsion between the template and residue 231 leading to the distortion of the dNTP binding pocket. In addition, expression of G231D was insufficient to rescue pol β-deficient cells treated with chemotherapeutic agents suggesting that these agents may be effectively used to treat tumors harboring this mutation. More importantly, this suggests that the G231D variant has impaired base excision repair. Together, these data indicate that the G231D variant plays a role in driving cancer.
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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.