ArticleOncogene2005
Tumor-prone phenotype of the DDB2-deficient mice.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 89 citations in OpenAlex.
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- New insights into keloid pathogenesis: biomarker potential for CDK7 and DDB2.Frontiers in cell and developmental biology · 2025Article
- Function, mechanism and drug discovery of ubiquitin and ubiquitin-like modification with multiomics profiling for cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- UV-DDB as a General Sensor of DNA Damage in Chromatin: Multifaceted Approaches to Assess Its Direct Role in Base Excision Repair.International journal of molecular sciences · 2023Review
- Can accelerated ageing models inform us on age-related tauopathies?Aging cell · 2023Review
- Cooperative interaction between AAG and UV-DDB in the removal of modified bases.Nucleic acids research · 2022Article
- A protein with broad functions: damage-specific DNA-binding protein 2.Molecular biology reports · 2022Review
- The role of UV-DDB in processing 8-oxoguanine during base excision repair.Biochemical Society transactions · 2022Review
- Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?Cell death and differentiation · 2022Review
- Exploiting Interdata Relationships in Prostate Cancer Proteomes: Clinical Significance of HO-1 Interactors.Antioxidants (Basel, Switzerland) · 2022Article
- Single molecule analysis indicates stimulation of MUTYH by UV-DDB through enzyme turnover.Nucleic acids research · 2021Article
- DDB2 regulates DNA replication through PCNA-independent degradation of CDT2.Cell & bioscience · 2021Article
- USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors.Frontiers in cell and developmental biology · 2021Article
- XPC deficiency increases risk of hematologic malignancies through mutator phenotype and characteristic mutational signature.Nature communications · 2020Article
- Review
- Article
- Losses of human disease-associated genes in placental mammals.NAR genomics and bioinformatics · 2020Article
- Association between Single-Nucleotide Polymorphism in MicroRNA Target Site ofBioMed research international · 2020Article
- Depletion of DNA damage binding protein 2 sensitizes triple-negative breast cancer cells to poly ADP-ribose polymerase inhibition by destabilizing Rad51.Cancer science · 2019Article
- Emerging Roles of DDB2 in Cancer.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
DDB2 is an essential subunit of the damaged-DNA recognition factor DDB, which is involved in global genomic repair in human cells. Moreover, DDB2 is mutated in the repair-deficiency disease xeroderma pigmentosum (Group E). Expression of DDB2 in human cells is induced by P53, BRCA1 and by ionizing radiation. The DDB2 protein associates with transcriptional activator and coactivator proteins. In addition, DDB2 in conjunction with DDB1 associates with cullin 4A and the Cop9/signalosome. We generated a mouse strain deficient for DDB2 (DDB2-/-). Consistent with the human disease (XP-E), the DDB2-/- mice were susceptible to UV-induced skin carcinogenesis. We observed a significant difference in the initial rate of cyclobutane pyrimidine dimer (CPD)-removal from the skin following UV irradiation. Also, the DDB2-deficient mice exhibited a significantly reduced life span compared to their wild-type littermates. Moreover, unlike other XP-deficient mice, the DDB2-deficient mice developed spontaneous malignant tumors at a high rate between the ages of 20 and 25 months. The observations suggest that, in addition to DNA repair, the other interactions of DDB2 are significant in its tumor suppression function.
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What OpenQuestion holds
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.