ReviewInternational journal of cancer2016
Transcription factors that interact with p53 and Mdm2.
Review in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 104 citations in OpenAlex.
- YY1 in prostate cancer: multidimensional oncogenicmechanisms and emerging therapeutic vulnerabilities.Journal of molecular histology · 2026Review
- Review
- Using transcription and translation regulators to improve recombinant protein expression in CHO cells.Acta biochimica et biophysica Sinica · 2025Article
- Development of CDK4/6 Inhibitors in Gastrointestinal Cancers: Biomarkers to Move Forward.Current issues in molecular biology · 2025Review
- KT-253, a Novel MDM2 Degrader and p53 Stabilizer, Has Superior Potency and Efficacy than MDM2 Small-Molecule Inhibitors.Molecular cancer therapeutics · 2025Article
- Ribosome biogenesis rate, a parameter of sensitivity to chemotherapeutic drugs inhibiting rRNA synthesis.Oncology reviews · 2025Review
- YBX1: A Multifunctional Protein in Senescence and Immune Regulation.Current issues in molecular biology · 2024Review
- Two-polarized roles of transcription factor FOSB in lung cancer progression and prognosis: dependent on p53 status.Journal of experimental & clinical cancer research : CR · 2024Article
- Delineating the mechanistic relevance of theHeliyon · 2024Article
- MDM2: current research status and prospects of tumor treatment.Cancer cell international · 2024Review
- Dysregulation of ubiquitination modification in renal cell carcinoma.Frontiers in genetics · 2024Review
- MDM2 Implications for Potential Molecular Pathogenic Therapies of Soft-Tissue Tumors.Journal of clinical medicine · 2023Review
- Specific regulation of BACH1 by the hotspot mutant p53Nature cancer · 2023Article
- Expression and Clinical Significance of MDM2 in Non-Functioning PitNETs.Medicina (Kaunas, Lithuania) · 2023Article
- Apoptotic pathway protein expression variance in metal oxide and quantum dot treated HeLa cells.microPublication biology · 2023Article
- PAHSAs reduce cellular senescence and protect pancreatic beta cells from metabolic stress through regulation of Mdm2/p53.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Novel Therapies in Myelofibrosis: Beyond JAK Inhibitors.Current hematologic malignancy reports · 2022Review
- Improved cognitive impairments by silencing DMP1 via enhancing the proliferation of neural progenitor cell in Alzheimer-like mice.Aging cell · 2022Article
- Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.International journal of molecular sciences · 2022Review
2 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor p53 is activated upon cellular stresses such as DNA damage, oncogene activation, hypoxia, which transactivates sets of genes that induce DNA repair, cell cycle arrest, apoptosis, or autophagy, playing crucial roles in the prevention of tumor formation. The central regulator of the p53 pathway is Mdm2 which inhibits transcriptional activity, nuclear localization and protein stability. More than 30 cellular p53-binding proteins have been isolated and characterized including Mdm2, Mdm4, p300, BRCA1/2, ATM, ABL and 53BP-1/2. Most of them are nuclear proteins; however, not much is known about p53-binding transcription factors. In this review, we focus on transcription factors that directly interact with p53/Mdm2 through direct binding including Dmp1, E2F1, YB-1 and YY1. Dmp1 and YB-1 bind only to p53 while E2F1 and YY1 bind to both p53 and Mdm2. Dmp1 has been shown to bind to p53 and block all the known functions for Mdm2 on p53 inhibition, providing a secondary mechanism for tumor suppression in Arf-null cells. Although E2F1-p53 binding provides a checkpoint mechanism to silence hyperactive E2F1, YB-1 or YY1 interaction with p53 subverts the activity of p53, contributing to cell cycle progression and tumorigenesis. Thus, the modes and consequences for each protein-protein interaction vary from the viewpoint of tumor development and suppression.
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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.