ArticleThe Journal of biological chemistry2010
MDM2 mediates ubiquitination and degradation of activating transcription factor 3.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Serine metabolism reprogramming in cancer: a multi-tiered regulatory framework.Acta biochimica et biophysica Sinica · 2025Review
- Osthole induces accumulation of impaired autophagosome against pancreatic cancer cells.Scientific reports · 2024Article
- A Legionella toxin exhibits tRNA mimicry and glycosyl transferase activity to target the translation machinery and trigger a ribotoxic stress response.Nature cell biology · 2023Article
- Improving the Antitumor Effect of Chemotherapy with Ocoxin as a Novel Adjuvant Agent to Treat Prostate Cancer.Nutrients · 2023Article
- Nuclear Receptor PXR Confers Irradiation Resistance by Promoting DNA Damage Response Through Stabilization of ATF3.Frontiers in oncology · 2022Article
- It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
- ATF3 promotes the serine synthesis pathway and tumor growth under dietary serine restriction.Cell reports · 2021Article
- The ATF3 Transcription Factor Is a Short-Lived Substrate of the Arg/N-Degron Pathway.Biochemistry · 2020Article
- Deleting key autophagy elongation proteins induces acquirement of tumor-associated phenotypes via ISG15.Cell death and differentiation · 2020Article
- Competitive ubiquitination activates the tumor suppressor p53.Cell death and differentiation · 2020Article
- Neddylation inhibition activates the protective autophagy through NF-κB-catalase-ATF3 Axis in human esophageal cancer cells.Cell communication and signaling : CCS · 2020Article
- Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells.PloS one · 2019Article
- Article
- Trans-chalcone increases p53 activity via DNAJB1/HSP40 induction and CRM1 inhibition.PloS one · 2018Article
- The Stress-responsive Gene ATF3 Mediates Dichotomous UV Responses by Regulating the Tip60 and p53 Proteins.The Journal of biological chemistry · 2016Article
- The common stress responsive transcription factor ATF3 binds genomic sites enriched with p300 and H3K27ac for transcriptional regulation.BMC genomics · 2016Article
- MDM2 Associates with Polycomb Repressor Complex 2 and Enhances Stemness-Promoting Chromatin Modifications Independent of p53.Molecular cell · 2016Article
- Emerging roles of ATF3 in the suppression of prostate cancer.Molecular & cellular oncology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Activating transcription factor 3 (ATF3) is a common stress sensor, and its rapid induction by cellular stresses (e.g. DNA damage) is crucial for cells to mount appropriate responses (e.g. activating the tumor suppressor p53) and maintain homeostasis. Although emerging evidence suggests that dysregulation of ATF3 contributes to occurrences of human diseases including cancer, the mechanism(s) by which ATF3 expression is regulated is largely unknown. Here, we demonstrate that mouse double minute 2 (MDM2) is a bona fide E3 ubiquitin ligase for ATF3 and regulates ATF3 expression by promoting its degradation. MDM2 via its C-terminal RING finger can bind to the Basic region of ATF3 and mediate the addition of ubiquitin moieties to the ATF3 leucine zipper domain. As a consequence, ATF3, but not a mutant deficient in MDM2 binding (Delta80-100), is degraded by MDM2-mediated proteolysis. Consistent with these results, ablation of MDM2 in cells not only increases basal ATF3 levels, but results in stabilization of ATF3 in late stages of DNA damage responses. Because ATF3 was recently identified as a p53 activator, these results suggest that MDM2 could inactivate p53 through an additional feedback mechanism involving ATF3. Therefore, we provide the first evidence demonstrating that ATF3 is regulated by a posttranslational mechanism.
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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.