Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence

International Journal of Molecular Sciences

Nilotpal Roy¹  Srilata Bagchi² 

[1] Department of Biochemistry and Molecular Genetics (M/C 669), University of Illinois at Chicago, 900 S. Ashland Ave, Chicago, IL 60607, USA; E-Mail:;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; E-Mail:

关键词: DDB2;    senescence;    reactive oxygen species;    apoptosis;    NER;   

DOI  :  10.3390/ijms130911012

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.