ArticleMolecular and cellular biology2010
The ATDC (TRIM29) protein binds p53 and antagonizes p53-mediated functions.
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. Cited by 75 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.
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Who cites it
75 citing papers in PubMed, 113 citations in OpenAlex.
- TRIM29 suppresses malignant progression in lung squamous cell carcinoma by shaping an immunosuppressive tumor microenvironment.Scientific reports · 2026Article
- TRIM69 alleviates ultraviolet B irradiation-induced ferroptosis by regulating p53 in human lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Article
- TRIM29 promotes bladder cancer invasion by regulating the intermediate filament network and focal adhesion.Oncogene · 2025Article
- Does side matter? Deciphering mechanisms that underpin side-dependent pathogenesis and therapy response in colorectal cancer.Molecular cancer · 2025Review
- Therapeutic potential of TRIM family proteins in gastric cancer: from signaling pathway regulation to precision targeting strategies.Frontiers in oncology · 2025Review
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- O-GlcNAcylation of TRIM29 and OGT translation forms a feedback loop to promote adaptive response of PDAC cells to glucose deficiency.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- TP63-TRIM29 axis regulates enhancer methylation and chromosomal instability in prostate cancer.Epigenetics & chromatin · 2024Article
- TRIM29 modulates proteins involved in PTEN/AKT/mTOR and JAK2/STAT3 signaling pathway and suppresses the progression of hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024Article
- Exploring the Mechanisms, Biomarkers, and Therapeutic Targets of TRIM Family in Gastrointestinal Cancer.Drug design, development and therapy · 2024Review
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TRIM29 acts as a potential senescence suppressor with epigenetic activation in nasopharyngeal carcinoma.Cancer science · 2023Article
- TRIM29 hypermethylation drives esophageal cancer progression via suppression of ZNF750.Cell death discovery · 2023Article
- TRIM29 knockdown prevented the colon cancer progression through decreasing the ubiquitination levels of KRT5.Open life sciences · 2023Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- TRIM3 and TRIM16 as potential tumor suppressors in breast cancer patients.BMC research notes · 2022Article
- Identification of a Novel Oncogenic Fusion GeneInternational journal of molecular sciences · 2022Article
- Targeting Post-Translational Regulation of p53 in Colorectal Cancer by Exploiting Vulnerabilities in the p53-MDM2 Axis.Cancers · 2022Review
- Identification of a tripartite motif family gene signature for predicting the prognosis of patients with glioma.American journal of translational research · 2022Article
- GH and Senescence: A New Understanding of Adult GH Action.Journal of the Endocrine Society · 2022Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The ataxia telangiectasia group D-complementing (ATDC) gene product, also known as TRIM29, is a member of the tripartite motif (TRIM) protein family. ATDC has been proposed to form homo- or heterodimers and to bind nucleic acids. In cell cultures, ATDC expression leads to rapid growth and resistance to ionizing radiation (IR), whereas silencing of ATDC expression decreases growth rates and increases sensitivity to IR. Although ATDC is overexpressed in many human cancers, the biological significance of ATDC overexpression remains obscure. We report here that ATDC increases cell proliferation via inhibition of p53 nuclear activities. ATDC represses the expression of p53-regulated genes, including p21 and NOXA. Mechanistically, ATDC binds p53, and this interaction is potentially fine-tuned by posttranslational acetylation of lysine 116 on ATDC. The association of p53 and ATDC results in p53 sequestration outside of the nucleus. Together, these results provide novel mechanistic insights into the function of ATDC and offer an explanation for how ATDC promotes cancer cell proliferation.
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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.