posted on 2013-12-05, 00:00authored byNilotpal Roy, Srilata Bagchi, Pradip Raychaudhuri
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.
Funding
PR and SB are supported by grants from the National Cancer Institute (CA 77637 and CA 156164).
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. doi: 10.3390/ijms130911012