Published in Mutat Res Genet Toxicol Environ Mutagen on July 04, 2015
Chromosome thripsis by DNA double strand break clusters causes enhanced cell lethality, chromosomal translocations and 53BP1-recruitment. Nucleic Acids Res (2016) 0.78
Alternative Okazaki Fragment Ligation Pathway by DNA Ligase III. Genes (Basel) (2015) 0.76
The DNA resection protein CtIP promotes mammary tumorigenesis. Oncotarget (2016) 0.75
Microhomology-mediated end joining is activated in irradiated human cells due to phosphorylation-dependent formation of the XRCC1 repair complex. Nucleic Acids Res (2016) 0.75
Novel Biological Approaches for Testing the Contributions of Single DSBs and DSB Clusters to the Biological Effects of High LET Radiation. Front Oncol (2016) 0.75
Chromatin organization revealed by nanostructure of irradiation induced γH2AX, 53BP1 and Rad51 foci. Sci Rep (2017) 0.75
Regulation of non-homologous end joining via post-translational modifications of components of the ligation step. Curr Genet (2016) 0.75
Alternative end-joining repair pathways are the ultimate backup for abrogated classical non-homologous end-joining and homologous recombination repair: Implications for the formation of chromosome translocations. Mutat Res Genet Toxicol Environ Mutagen (2015) 0.97
Bystander effects as manifestation of intercellular communication of DNA damage and of the cellular oxidative status. Cancer Lett (2013) 0.88
Role for Artemis nuclease in the repair of radiation-induced DNA double strand breaks by alternative end joining. DNA Repair (Amst) (2015) 0.78