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Unicellular organisms respond to the presence of DNA lesions by activating cell cycle checkpoint and repair mechanisms, while multicellular animals have acquired the further option of eliminating damaged cells by triggering apoptosis. Defects in DNA damage-induced apoptosis contribute to tumorigenesis and to the resistance of cancer cells to a variety of therapeutic agents. The intranuclear mechanisms that signal apoptosis after DNA damage overlap with those that initiate cell cycle arrest and DNA repair, and the early events in these pathways are highly conserved. In addition, multiple independent routes have recently been traced by which nuclear DNA damage can be signalled to the mitochondria, tipping the balance in favour of cell death rather than repair and survival. Here, we review current knowledge of nuclear DNA damage signalling, giving particular attention to interactions between these nuclear events and apoptotic processes in other intracellular compartments.

Original publication

DOI

10.1038/sj.onc.1207532

Type

Journal article

Journal

Oncogene

Publication Date

12/04/2004

Volume

23

Pages

2797 - 2808

Keywords

Adaptor Proteins, Signal Transducing, Animals, Apoptosis, Ataxia Telangiectasia Mutated Proteins, Carrier Proteins, Caspase 2, Caspases, Cell Cycle Proteins, Cell Survival, DNA Damage, DNA Repair, DNA-Activated Protein Kinase, DNA-Binding Proteins, Fas-Associated Death Domain Protein, Histones, Humans, Nuclear Proteins, Protein-Serine-Threonine Kinases, Tumor Suppressor Protein p53