ArticleMolecular and cellular biology1998
Alkylpurine-DNA-N-glycosylase knockout mice show increased susceptibility to induction of mutations by methyl methanesulfonate.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 113 citations in OpenAlex.
- The DNA Alkyltransferase Family of DNA Repair Proteins: Common Mechanisms, Diverse Functions.International journal of molecular sciences · 2023Review
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Versatile cell-based assay for measuring DNA alkylation damage and its repair.Scientific reports · 2021Article
- The marker of alkyl DNA base damage, N7-methylguanine, is associated with semen quality in men.Scientific reports · 2021Article
- Incomplete base excision repair contributes to cell death from antibiotics and other stresses.DNA repair · 2018Review
- Base excision repair imbalance in colorectal cancer has prognostic value and modulates response to chemotherapy.Oncotarget · 2017Article
- ATM regulates 3-methylpurine-DNA glycosylase and promotes therapeutic resistance to alkylating agents.Cancer discovery · 2014Article
- DNA breaks and chromosomal aberrations arise when replication meets base excision repair.The Journal of cell biology · 2014Article
- Base excision repair and cancer.Cancer letters · 2012Review
- Alkylation sensitivity screens reveal a conserved cross-species functionome.Molecular cancer research : MCR · 2012Article
- Balancing repair and tolerance of DNA damage caused by alkylating agents.Nature reviews. Cancer · 2012Review
- Detection of PIGO-deficient cells using proaerolysin: a valuable tool to investigate mechanisms of mutagenesis in the DT40 cell system.PloS one · 2012Article
- Formation and repair of tobacco carcinogen-derived bulky DNA adducts.Journal of nucleic acids · 2010Article
- Kinetic mechanism for the flipping and excision of 1,N(6)-ethenoadenine by human alkyladenine DNA glycosylase.Biochemistry · 2009Article
- Cells deficient in PARP-1 show an accelerated accumulation of DNA single strand breaks, but not AP sites, over the PARP-1-proficient cells exposed to MMS.Mutation research · 2009Article
- Recognition and processing of a new repertoire of DNA substrates by human 3-methyladenine DNA glycosylase (AAG).Biochemistry · 2009Article
- YNK1, the yeast homolog of human metastasis suppressor NM23, is required for repair of UV radiation- and etoposide-induced DNA damage.Mutation research · 2009Article
- Human methyl purine DNA glycosylase and DNA polymerase beta expression collectively predict sensitivity to temozolomide.Molecular pharmacology · 2008Article
- Eukaryotic Y-family polymerases bypass a 3-methyl-2'-deoxyadenosine analog in vitro and methyl methanesulfonate-induced DNA damage in vivo.Nucleic acids research · 2008Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alkylpurine-DNA-N-glycosylase (APNG) null mice have been generated by homologous recombination in embryonic stem cells. The null status of the animals was confirmed at the mRNA level by reverse transcription-PCR and by the inability of cell extracts of tissues from the knockout (ko) animals to release 3-methyladenine (3-meA) or 7-methylguanine (7-meG) from 3H-methylated calf thymus DNA in vitro. Following treatment with DNA-methylating agents, increased persistence of 7-meG was found in liver sections of APNG ko mice in comparison with wild-type (wt) mice, demonstrating an in vivo phenotype for the APNG null animals. Unlike other null mutants of the base excision repair pathway, the APNG ko mice exhibit a very mild phenotype, show no outward abnormalities, are fertile, and have an apparently normal life span. Neither a difference in the number of leukocytes in peripheral blood nor a difference in the number of bone marrow polychromatic erythrocytes was found when ko and wt mice were exposed to methylating or chloroethylating agents. These agents also showed similar growth-inhibitory effects in primary embryonic fibroblasts isolated from ko and wt mice. However, treatment with methyl methanesulfonate resulted in three- to fourfold more hprt mutations in splenic T lymphocytes from APNG ko mice than in those from wt mice. These mutations were predominantly single-base-pair changes; in the ko mice, they consisted primarily of AT-->TA and GC-->TA transversions, which most likely are caused by 3-meA and 3- or 7-meG, respectively. These results clearly show an important role for APNG in attenuating the mutagenic effects of N-alkylpurines in vivo.
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