ArticleProceedings of the National Academy of Sciences of the United States of America2004
DDB2 gene disruption leads to skin tumors and resistance to apoptosis after exposure to ultraviolet light but not a chemical carcinogen.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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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
48 citing papers in PubMed, 96 citations in OpenAlex.
- Genetic Structure and Selective Signature Analysis of Xinjiang Local Sheep Populations.Animals : an open access journal from MDPI · 2026Article
- 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
- Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?Cell death and differentiation · 2022Review
- USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors.Frontiers in cell and developmental biology · 2021Article
- Review
- Article
- Losses of human disease-associated genes in placental mammals.NAR genomics and bioinformatics · 2020Article
- Damage sensor role of UV-DDB during base excision repair.Nature structural & molecular biology · 2019Article
- Tissue specificity of DNA damage response and tumorigenesis.Cancer biology & medicine · 2019Article
- Regulation of liver receptor homologue-1 by DDB2 E3 ligase activity is critical for hepatic glucose metabolism.Scientific reports · 2019Article
- A Recurrent ERCC3 Truncating Mutation Confers Moderate Risk for Breast Cancer.Cancer discovery · 2016Article
- Association of nucleotide excision repair pathway gene polymorphisms with gastric cancer and atrophic gastritis risks.Oncotarget · 2016Article
- Global-genome Nucleotide Excision Repair Controlled by Ubiquitin/Sumo Modifiers.Frontiers in genetics · 2016Review
- Orchestral maneuvers at the damaged sites in nucleotide excision repair.Cellular and molecular life sciences : CMLS · 2015Review
- Functional regulation of the DNA damage-recognition factor DDB2 by ubiquitination and interaction with xeroderma pigmentosum group C protein.Nucleic acids research · 2015Article
- Dual role of SIRT1 in UVB-induced skin tumorigenesis.Oncogene · 2015Article
- Chromatin retention of DNA damage sensors DDB2 and XPC through loss of p97 segregase causes genotoxicity.Nature communications · 2014Article
- The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the human DDB2 gene give rise to xeroderma pigmentosum group E, a disease characterized by increased skin tumorigenesis in response to UV-irradiation. Cell strains derived from xeroderma pigmentosum group E individuals also have enhanced resistance to UV-irradiation due to decreased p53-mediated apoptosis. To further address the precise function(s) of DDB2 and the consequence of non-naturally occurring DDB2 mutations, we generated mice with a disruption of the gene. The mice exhibited significantly enhanced skin carcinogenesis in response to UV-irradiation, and cells from the DDB2(-/-) mice were abnormally resistant to killing by the radiation and had diminished UV-induced, p53-mediated apoptosis. Notably, the cancer-prone phenotype and the resistance to cellular killing were not observed after exposure to the chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), to which mice carrying defective nucleotide excision repair genes respond with enhanced tumors and cell killing. Although cells from heterozygous DDB2(+/-) mice appeared normal, these mice had enhanced skin carcinogenesis after UV-irradiation, so that XP-E heterozygotes might be at risk for carcinogenesis. In sum, these results demonstrate that DDB2 is well conserved between humans and mice and functions as a tumor suppressor, at least in part, by controlling p53-mediated apoptosis after UV-irradiation.
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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.