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Chemical biology of mutagenesis and DNA repair: cellular responses to DNA alkylation.

TLDR
The respective contributions of specific DNA lesions to the biological effects of low molecular weight alkylating agents are described.
Abstract
The reaction of DNA-damaging agents with the genome results in a plethora of lesions, commonly referred to as adducts. Adducts may cause DNA to mutate, they may represent the chemical precursors of lethal events and they can disrupt expression of genes. Determination of which adduct is responsible for each of these biological endpoints is difficult, but this task has been accomplished for some carcinogenic DNA-damaging agents. Here, we describe the respective contributions of specific DNA lesions to the biological effects of low molecular weight alkylating agents.

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Journal ArticleDOI

Balancing repair and tolerance of DNA damage caused by alkylating agents

TL;DR: In this article, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylation agent toxicity.
Journal ArticleDOI

β-lactam antibiotics promote bacterial mutagenesis via an RpoS-mediated reduction in replication fidelity

TL;DR: It is shown that mutagenesis induced by subinhibitory concentrations of antibiotics is a genetically controlled process that should be taken into consideration for the development of more efficient antimicrobial therapeutic strategies.
Journal ArticleDOI

DNA damage by reactive species: Mechanisms, mutation and repair

TL;DR: This review provides an overview of different guanine lesions formed due to reactions of Guanine with different reactive species, including involvement of these lesions in inter- and intra-strand crosslinks, DNA–protein crosslinks and mutagenesis.
Journal ArticleDOI

The AlkB Family of Fe(II)/α-Ketoglutarate-dependent Dioxygenases: Repairing Nucleic Acid Alkylation Damage and Beyond

TL;DR: This minireview presents an overview of the AlkB proteins including recent data on homologs, structural features, substrate specificities, and experimental strategies for studying DNA repair by AlkB family proteins.
Journal ArticleDOI

DNA damage and repair in plants - from models to crops.

TL;DR: Enhanced understanding of DNA repair processes in plants will inform and accelerate the engineering of crop genomes via both traditional and targeted approaches.
References
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
Journal ArticleDOI

Beyond aerobic glycolysis : Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis

TL;DR: Transformed cells exhibit a high rate of glutamine consumption that cannot be explained by the nitrogen demand imposed by nucleotide synthesis or maintenance of nonessential amino acid pools, and glutamine metabolism provides a carbon source that facilitates the cell's ability to use glucose-derived carbon and TCA cycle intermediates as biosynthetic precursors.
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Oxyradicals and DNA damage

TL;DR: The levels of oxidative DNA damage reported in many human tissues or in animal models of carcinogenesis exceed the levels of lesions induced by exposure to exogenous carcinogenic compounds, and it seems likely that oxidativeDNA damage is important in the etiology of many human cancers.
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