IFC(EDITORIAL BOARD)
Published in DNA Repair
Mass spectrometry-based quantification of the cellular response to methyl methanesulfonate treatment in human cells
Published in DNA Repair
Faithful transmission of genetic material is essential for cell viability and organism health. The occurrence of DNA damage, due to either spontaneous events or environmental agents, threatens the integrity of the genome. The consequences of these insults, if allowed to perpetuate and accumulate over time, are mutations that can lead to the develop...
In memory of John Bruce Hays (1937–2014)
Published in DNA Repair
Structures of the Leishmania infantum polymerase beta
Published in DNA Repair
Protozoans of the genus Leishmania, the pathogenic agent causing leishmaniasis, encode the family X DNA polymerase Li Pol β. Here, we report the first crystal structures of Li Pol β. Our pre- and post-catalytic structures show that the polymerase adopts the common family X DNA polymerase fold. However, in contrast to other family X DNA polymerases,...
In vivo evidence that phenylalanine 171 acts as a molecular brake for translesion DNA synthesis across benzo[a]pyrene DN...
...Published in DNA Repair
Humans possess multiple specialized DNA polymerases that continue DNA replication beyond a variety of DNA lesions. DNA polymerase kappa (Pol κ) bypasses benzo[a]pyrene diolepoxide-N2-deoxyguanine (BPDE-N2-dG) DNA adducts in an almost error-free manner. In the previous work, we changed the amino acids close to the adducts in the active site and exam...
Section on Databases, Methods and New Technologies
Published in DNA Repair
The distribution of DNA damage is defined by region-specific susceptibility to DNA damage formation rather than repair d...
Published in DNA Repair
The cellular genomes are continuously damaged by reactive oxygen species (ROS) from aerobic processes. The impact of DNA damage depends on the specific site as well as the cellular state. The steady-state level of DNA damage is the net result of continuous formation and subsequent repair, but it is unknown to what extent heterogeneous damage distri...
Alternative end-joining pathway(s): Bricolage at DNA breaks
Published in DNA Repair
To cope with DNA double strand break (DSB) genotoxicity, cells have evolved two main repair pathways: homologous recombination which uses homologous DNA sequences as repair templates, and non-homologous Ku-dependent end-joining involving direct sealing of DSB ends by DNA ligase IV (Lig4). During the last two decades a third player most commonly nam...
Do genetic factors protect for early onset lung cancer? A case control study before the age of 50 years
...Published in BMC Cancer
BackgroundEarly onset lung cancer shows some familial aggregation, pointing to a genetic predisposition. This study was set up to investigate the role of candidate genes in the susceptibility to lung cancer patients younger than 51 years at diagnosis.Methods246 patients with a primary, histologically or cytologically confirmed neoplasm, recruited f...
DNA-PK: A dynamic enzyme in a versatile DSB repair pathway
Published in DNA Repair
DNA double stranded breaks (DSBs) are the most cytoxic DNA lesion as the inability to properly repair them can lead to genomic instability and tumorigenesis. The prominent DSB repair pathway in humans is non-homologous end-joining (NHEJ). In the simplest sense, NHEJ mediates the direct re-ligation of the broken DNA molecule. However, NHEJ is a comp...
