ArticleMolecular and cellular biology2010
DDB2, an essential mediator of premature senescence.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- New insights into keloid pathogenesis: biomarker potential for CDK7 and DDB2.Frontiers in cell and developmental biology · 2025Article
- Article
- A protein with broad functions: damage-specific DNA-binding protein 2.Molecular biology reports · 2022Review
- Inhibition of miR-328-3p Impairs Cancer Stem Cell Function and Prevents Metastasis in Ovarian Cancer.Cancer research · 2019Article
- DDB2 represses ovarian cancer cell dedifferentiation by suppressing ALDH1A1.Cell death & disease · 2018Article
- Article
- Chromatin association of XRCC5/6 in the absence of DNA damage depends on the XPE gene product DDB2.Molecular biology of the cell · 2017Article
- DDB2 increases radioresistance of NSCLC cells by enhancing DNA damage responses.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The emerging role of deubiquitination in nucleotide excision repair.DNA repair · 2016Review
- Gadd45b deficiency promotes premature senescence and skin aging.Oncotarget · 2016Article
- Oxidative stress and age-related changes in T cells: is thalassemia a model of accelerated immune system aging?Central-European journal of immunology · 2016Review
- DDB2 modulates TGF-β signal transduction in human ovarian cancer cells by downregulating NEDD4L.Nucleic acids research · 2015Article
- Essential roles of FoxM1 in Ras-induced liver cancer progression and in cancer cells with stem cell features.Journal of hepatology · 2015Article
- A DDB2 mutant protein unable to interact with PCNA promotes cell cycle progression of human transformed embryonic kidney cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Protein kinase D1 is essential for Ras-induced senescence and tumor suppression by regulating senescence-associated inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- DDB2 suppresses tumorigenicity by limiting the cancer stem cell population in ovarian cancer.Molecular cancer research : MCR · 2014Article
- Chromatin retention of DNA damage sensors DDB2 and XPC through loss of p97 segregase causes genotoxicity.Nature communications · 2014Article
- DNA damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.Molecular cancer research : MCR · 2014Article
- Cellular senescence and protein degradation: breaking down cancer.Cell cycle (Georgetown, Tex.) · 2014Article
- Interferon-γ induces senescence in normal human melanocytes.PloS one · 2014Article
Corrections and comments
- Retraction · 2017-06-01Duplication of/in Image ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) is critical for premature senescence, a process significant in tumor suppression and cancer therapy. Here, we reveal a novel function of the nucleotide excision repair protein DDB2 in the accumulation of ROS in a manner that is essential for premature senescence. DDB2-deficient cells fail to undergo premature senescence induced by culture shock, exogenous oxidative stress, oncogenic stress, or DNA damage. These cells do not accumulate ROS following DNA damage. The lack of ROS accumulation in DDB2 deficiency results from high-level expression of the antioxidant genes in vitro and in vivo. DDB2 represses antioxidant genes by recruiting Cul4A and Suv39h and by increasing histone-H3K9 trimethylation. Moreover, expression of DDB2 also is induced by ROS. Together, our results show that, upon oxidative stress, DDB2 functions in a positive feedback loop by repressing the antioxidant genes to cause persistent accumulation of ROS and induce premature senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.