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Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
Department of Biochemistry and Molecular Genetics (M/C 669), University of Illinois at Chicago, 900 S. Ashland Ave, Chicago, IL 60607, USA
Center of Molecular Biology of Oral Diseases (M/C 860), College of Dentistry, Cancer Center, University of Illinois at Chicago, 801 S. Paulina Ave, Chicago, IL 60612, USA
* Author to whom correspondence should be addressed.
Received: 6 August 2012; in revised form: 22 August 2012 / Accepted: 28 August 2012 / Published: 5 September 2012
Abstract: Premature senescence induced by DNA damage or oncogene is a critical mechanism of tumor suppression. Reactive oxygen species (ROS) have been implicated in the induction of premature senescence response. Several pathological disorders such as cancer, aging and age related neurological abnormalities have been linked to ROS deregulation. Here, we discuss how Damaged DNA binding Protein-2 (DDB2), a nucleotide excision repair protein, plays an important role in ROS regulation by epigenetically repressing the antioxidant genes MnSOD and Catalase. We further revisit a model in which DDB2 plays an instrumental role in DNA damage induced ROS accumulation, ROS induced premature senescence and inhibition of skin tumorigenesis.
Keywords: DDB2; senescence; reactive oxygen species; apoptosis; NER
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Roy, N.; Bagchi, S.; Raychaudhuri, P. Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence. Int. J. Mol. Sci. 2012, 13, 11012-11026.
Roy N, Bagchi S, Raychaudhuri P. Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence. International Journal of Molecular Sciences. 2012; 13(9):11012-11026.
Roy, Nilotpal; Bagchi, Srilata; Raychaudhuri, Pradip. 2012. "Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence." Int. J. Mol. Sci. 13, no. 9: 11012-11026.