Nonhomologous end joining drives poly(ADP-ribose) polymerase (PARP) inhibitor lethality in homologous recombination-deficient cells

Poly(ADP-ribose) polymerase (PARP) inhibitors are strikingly toxic to cells with defects in homologous recombination (HR). The mechanistic basis for these findings is incompletely understood. Here, we show that PARP inhibitor treatment induces phosphorylation of DNA-dependent protein kinase substrat...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2011-02, Vol.108 (8), p.3406-3411
Hauptverfasser:	Patel, Anand G., Sarkaria, Jann N., Kaufmann, Scott H., Hanawalt, Philip C.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological Sciences BRCA1 protein BRCA2 protein Cell Death Cell Line Cell lines Cells Cytotoxicity Deoxyribonucleic acid DNA DNA damage DNA Repair DNA-Activated Protein Kinase - metabolism DNA-dependent protein kinase Enzyme Inhibitors - pharmacology Genetic mutation Genomic Instability Genomics homologous recombination Kinases Lethality Medical genetics Mice Non-homologous end joining Phosphorylation Poly(ADP-ribose) polymerase poly(ADP-ribose) polymerase 1 Poly(ADP-ribose) Polymerase Inhibitors Recombination, Genetic Small interfering RNA Somatic cells Toxicity Tumors
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