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

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 h...

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Detalles Bibliográficos
Autores principales: Roy, Nilotpal, Bagchi, Srilata, Raychaudhuri, Pradip
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472727/
https://www.ncbi.nlm.nih.gov/pubmed/23109835
http://dx.doi.org/10.3390/ijms130911012
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author Roy, Nilotpal
Bagchi, Srilata
Raychaudhuri, Pradip
author_facet Roy, Nilotpal
Bagchi, Srilata
Raychaudhuri, Pradip
author_sort Roy, Nilotpal
collection PubMed
description 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.
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spelling pubmed-34727272012-10-29 Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence Roy, Nilotpal Bagchi, Srilata Raychaudhuri, Pradip Int J Mol Sci Review 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. Molecular Diversity Preservation International (MDPI) 2012-09-05 /pmc/articles/PMC3472727/ /pubmed/23109835 http://dx.doi.org/10.3390/ijms130911012 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 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/).
spellingShingle Review
Roy, Nilotpal
Bagchi, Srilata
Raychaudhuri, Pradip
Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title_full Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title_fullStr Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title_full_unstemmed Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title_short Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence
title_sort damaged dna binding protein 2 in reactive oxygen species (ros) regulation and premature senescence
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472727/
https://www.ncbi.nlm.nih.gov/pubmed/23109835
http://dx.doi.org/10.3390/ijms130911012
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