To repair or not to repair? The endogenous role of human AlkB homologs and their association to obesity and cancer

• Applicant: Dr. Alexander Wolf
• Subject Area: Biochemistry
• Term: Funded in 2010
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 179222339

Deoxyribonucleic acid (DNA) is the genetic code that contains all the instructions required for the development and function of living organisms. The maintenance of genomic integrity is essential for the survival of a cell. But lesions in DNA can result from endogenous compounds or environmental agents, e.g. tobacco-specific nitrosamines, which can introduce cytotoxic mutations. To prevent the lethal and mutagenic effects of such damage, repair mechanisms have evolved that are highly conserved throughout evolution. In 2002 a novel mechanism to directly repair alkylated DNA was discovered in Escherichia coli: oxidative demethylation by the AlkB protein. In recent years, nine AlkB homologs have been identified in humans. The endogenous role of these proteins is so far unclear, but evidence has emerged suggesting associations with obesity, diabetes and cancer. The role of these potential repair enzymes in human cells and their involvement in obesity, diabetes and cancer are the main targets of this project.

• DFG Programme: Research Fellowships
• International Connection: United Kingdom
• Host: Professor Dr. Christopher J. Schofield