Featured Publications
Proton Irradiation Increases the Necessity for Homologous Recombination Repair Along with the Indispensability of Non-Homologous End Joining
Szymonowicz K, Krysztofiak A, van der Linden J, Kern A, Deycmar S, Oeck S, Squire A, Koska B, Hlouschek J, Vüllings M, Neander C, Siveke J, Matschke J, Pruschy M, Timmermann B, Jendrossek V. Proton Irradiation Increases the Necessity for Homologous Recombination Repair Along with the Indispensability of Non-Homologous End Joining. Cells 2020, 9: 889. PMID: 32260562, PMCID: PMC7226794, DOI: 10.3390/cells9040889.Peer-Reviewed Original Research
2018
Restraining Akt1 Phosphorylation Attenuates the Repair of Radiation-Induced DNA Double-Strand Breaks and Reduces the Survival of Irradiated Cancer Cells
Szymonowicz K, Oeck S, Krysztofiak A, van der Linden J, Iliakis G, Jendrossek V. Restraining Akt1 Phosphorylation Attenuates the Repair of Radiation-Induced DNA Double-Strand Breaks and Reduces the Survival of Irradiated Cancer Cells. International Journal Of Molecular Sciences 2018, 19: 2233. PMID: 30065170, PMCID: PMC6121313, DOI: 10.3390/ijms19082233.Peer-Reviewed Original ResearchConceptsDSB repairLong-term colony formation assaysDNA double-strand break repairDouble-strand break repairKinase-protein kinase BPhosphorylation-deficient mutantKey phosphorylation sitesDNA damage responseEssential subcellular processesProtein kinase BDSB repair kineticsCancer cellsCellular radiation responseActivation stateMurine prostate cancer cellsColony formation assaysEffector proteinsGenotoxic stressPhosphorylation sitesDamage responseBreak repairGenetic approachesThreonine 308Serine 473Kinase B