ArticleThe EMBO journal1996
Repair-deficient 3-methyladenine DNA glycosylase homozygous mutant mouse cells have increased sensitivity to alkylation-induced chromosome damage and cell killing.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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Who cites it
55 citing papers in PubMed, 186 citations in OpenAlex.
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Excision of mutagenic replication-blocking lesions suppresses cancer but promotes cytotoxicity and lethality in nitrosamine-exposed mice.Cell reports · 2021Article
- Mild phenotype of knockouts of the major apurinic/apyrimidinic endonuclease APEX1 in a non-cancer human cell line.PloS one · 2021Article
- Focus on DNA Glycosylases-A Set of Tightly Regulated Enzymes with a High Potential as Anticancer Drug Targets.International journal of molecular sciences · 2020Review
- Biological Basis for Threshold Responses to Methylating Agents.Chemical research in toxicology · 2020Review
- Molecular characterization of Plasmodium falciparum DNA-3-methyladenine glycosylase.Malaria journal · 2020Article
- Mutational convergence acts as a major player in adaptive parallel evolution of Shigella spp.Scientific reports · 2019Article
- Incomplete base excision repair contributes to cell death from antibiotics and other stresses.DNA repair · 2018Review
- APNG as a prognostic marker in patients with glioblastoma.PloS one · 2017Article
- Roles of Aag, Alkbh2, and Alkbh3 in the Repair of Carboxymethylated and Ethylated Thymidine Lesions.ACS chemical biology · 2016Article
- Abundance of BER-related proteins depends on cell proliferation status and the presence of DNA polymerase β.Journal of radiation research · 2015Article
- AP endonuclease knockdown enhances methyl methanesulfonate hypersensitivity of DNA polymerase β knockout mouse embryonic fibroblasts.Journal of radiation research · 2015Article
- Germ line variants of human N-methylpurine DNA glycosylase show impaired DNA repair activity and facilitate 1,N6-ethenoadenine-induced mutations.The Journal of biological chemistry · 2015Article
- ATM regulates 3-methylpurine-DNA glycosylase and promotes therapeutic resistance to alkylating agents.Cancer discovery · 2014Article
- NEIL1 responds and binds to psoralen-induced DNA interstrand crosslinks.The Journal of biological chemistry · 2013Article
- Base excision repair and cancer.Cancer letters · 2012Review
- Replication of the 2,6-diamino-4-hydroxy-N(5)-(methyl)-formamidopyrimidine (MeFapy-dGuo) adduct by eukaryotic DNA polymerases.Chemical research in toxicology · 2012Article
- Identification and characterization of human apurinic/apyrimidinic endonuclease-1 inhibitors.Biochemistry · 2012Article
- A model for 3-methyladenine recognition by 3-methyladenine DNA glycosylase I (TAG) from Staphylococcus aureus.Acta crystallographica. Section F, Structural biology and crystallization communications · 2012Article
- Balancing repair and tolerance of DNA damage caused by alkylating agents.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In Escherichia coli, the repair of 3-methyladenine (3MeA) DNA lesions prevents alkylation-induced cell death because unrepaired 3MeA blocks DNA replication. Whether this lesion is cytotoxic to mammalian cells has been difficult to establish in the absence of 3MeA repair-deficient cell lines. We previously isolated and characterized a mouse 3MeA DNA glycosylase cDNA (Aag) that provides resistance to killing by alkylating agents in E. coli. To determine the in vivo role of Aag, we cloned a large fragment of the Aag gene and used it to create Aag-deficient mouse cells by targeted homologous recombination. Aag null cells have no detectable Aag transcripts or 3MeA DNA glycosylase activity. The loss of Aag renders cells significantly more sensitive to methyl methanesulfonate-induced chromosome damage, and to cell killing induced by two methylating agents, one of which produces almost exclusively 3MeAs. Aag null embryonic stem cells become sensitive to two cancer chemotherapeutic alkylating agents, namely 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C, indicating that Aag status is an important determinant of cellular resistance to these agents. We conclude that this mammalian 3MeA DNA glycosylase plays a pivotal role in preventing alkylation-induced chromosome damage and cytotoxicity.
Indexed as
Identifiers
8631315PMC450292W236769407What OpenQuestion holds
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.