Nucleic Acids Res 2018 Jan;46(2):730-747
Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
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DNA Repair (Amst) 2010 Dec 30;9(12):1273-82. Epub 2010 Oct 30.
Genome Damage and Stability Centre, University of Sussex, East Sussex BN1 9RQ, United Kingdom.
DNA non-homologous end-joining (NHEJ) and homologous recombination (HR) represent the major DNA double strand break (DSB) pathways in mammalian cells, whilst ataxia telangiectasia mutated (ATM) lies at the core of the DSB signalling response. ATM signalling plays a major role in modifying chromatin structure in the vicinity of the DSB and increasing evidence suggests that this function influences the DSB rejoining process. DSBs have long been known to be repaired with two (or more) component kinetics. Read More
Nucleic Acids Res 2015 May 8;43(9):4517-30. Epub 2015 Apr 8.
The David and Inez Myers Laboratory for Cancer Research, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, George S. Wise Faculty of Life sciences, Tel Aviv University, Tel Aviv, 69978 Israel
The DNA damage response is vigorously activated by DNA double-strand breaks (DSBs). The chief mobilizer of the DSB response is the ATM protein kinase. We discovered that the COP9 signalosome (CSN) is a crucial player in the DSB response and an ATM target. Read More
PLoS One 2010 Apr 2;5(4):e10001. Epub 2010 Apr 2.
Department of Radiation Oncology, Virginia Commonwealth University, Richmond, Virginia, USA.
The DNA double-strand break (DSB) is the most toxic form of DNA damage. Studies aimed at characterizing DNA repair during development suggest that homologous recombination repair (HRR) is more critical in pluripotent cells compared to differentiated somatic cells in which nonhomologous end joining (NHEJ) is dominant. We have characterized the DNA damage response (DDR) and quality of DNA double-strand break (DSB) repair in human embryonic stem cells (hESCs), and in vitro-derived neural cells. Read More
Cell Cycle 2014 ;13(16):2509-16
a Department of Biophysics ; GSI Helmholtzzentrum für Schwerionenforschung GmbH ; Planckstraße 1; Darmstadt , Germany.
Repair of DNA double strand breaks (DSBs) is influenced by the chemical complexity of the lesion. Clustered lesions (complex DSBs) are generally considered more difficult to repair and responsible for early and late cellular effects after exposure to genotoxic agents. Resection is commonly used by the cells as part of the homologous recombination (HR) pathway in S- and G2-phase. Read More