Ralf Strasser

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Living organisms protect the genome against external influences by recognizing and repairing damaged DNA. A common source of gene mutation is the oxidized guanine, which undergoes base excision repair through cleavage of the glycosidic bond between the ribose and the nucleobase of the lesion. We unravel the repair mechanism utilized by bacterial(More)
Nucleotide excision repair (NER) is responsible for the removal of a large variety of structurally diverse DNA lesions. Mutations of the involved proteins cause the xeroderma pigmentosum (XP) cancer predisposition syndrome. Although the general mechanism of the NER process is well studied, the function of the XPA protein, which is of central importance for(More)
An investigation of the precise interactions between damaged DNA and DNA repair enzymes is required in order to understand the lesion recognition step, which is one of the most fundamental processes in DNA repair. Most recently, photoaffinity labeling approaches have enabled the analysis of even transient protein-DNA interactions. Here we report the(More)
Our genome is constantly damaged by exogenous and endogenous events. Particularly problematic is oxidative DNA damage caused by the reaction of reactive oxygen species (ROS) with the genetic material. The most common oxidative lesions are 8-oxodG and FaPy-dG. Repair of both lesions is essential for the survival of cells ; unrepaired lesions induce cell(More)
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