Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
journal contributionposted on 2013-12-05, 00:00 authored by Nilotpal 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.
PR and SB are supported by grants from the National Cancer Institute (CA 77637 and CA 156164).
Publisher Statement© 2012 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). The original version is available through MDPI at DOI: doi: 10.3390/ijms130911012.
CitationRoy 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