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Int. J. Mol. Sci. 2012, 13(9), 11012-11026; doi:10.3390/ijms130911012

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 / Revised: 22 August 2012 / Accepted: 28 August 2012 / Published: 5 September 2012
(This article belongs to the Special Issue DNA Damage and Repair in Degenerative Diseases)
View Full-Text   |   Download PDF [308 KB, 19 June 2014; original version 19 June 2014]   |  


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 DDB2; senescence; reactive oxygen species; apoptosis; NER
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

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.

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