ArticlePharmaceuticals (Basel, Switzerland)2010
Controlling the Mdm2-Mdmx-p53 Circuit.
Article in Pharmaceuticals (Basel, Switzerland), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Clinical utility of anti-p53 auto-antibody: systematic review and focus on colorectal cancer.World journal of gastroenterology · 2013Pooled it
- Targeting the ubiquitin-proteasome system: a novel therapeutic strategy for neuroblastoma.Frontiers in oncology · 2024Review
- Structure-Activity Relationship Studies of Chalcones and Diarylpentanoids with Antitumor Activity: Potency and Selectivity Optimization.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Understanding the interaction of 14-3-3 proteins with hDMX and hDM2: a structural and biophysical study.The FEBS journal · 2022Article
- The fate of murine double minute X (MdmX) is dictated by distinct signaling pathways through murine double minute 2 (Mdm2).Oncotarget · 2017Article
- Cisplatin causes cell death via TAB1 regulation of p53/MDM2/MDMX circuitry.Genes & development · 2013Article
- Mathematical model of dynamic protein interactions regulating p53 protein stability for tumor suppression.Computational and mathematical methods in medicine · 2013Article
- Selective Dual Inhibitors of the Cancer-Related Deubiquitylating Proteases USP7 and USP47.ACS medicinal chemistry letters · 2012Article
- Regulation of p53: a collaboration between Mdm2 and Mdmx.Oncotarget · 2012Review
- Induction of apoptotic genes by a p73-phosphatase and tensin homolog (p73-PTEN) protein complex in response to genotoxic stress.The Journal of biological chemistry · 2011Article
- Phosphodiesterase 3A (PDE3A) deletion suppresses proliferation of cultured murine vascular smooth muscle cells (VSMCs) via inhibition of mitogen-activated protein kinase (MAPK) signaling and alterations in critical cell cycle regulatory proteins.The Journal of biological chemistry · 2011Article
- Protein nitration and nitrosylation by NO-donating aspirin in colon cancer cells: Relevance to its mechanism of action.Experimental cell research · 2011Article
- c-Abl phosphorylation of Mdm2 facilitates Mdm2-Mdmx complex formation.The Journal of biological chemistry · 2011Article
- Critical role of VCP/p97 in the pathogenesis and progression of non-small cell lung carcinoma.PloS one · 2011Article
- Mdm2 links genotoxic stress and metabolism to p53.Protein & cell · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor is a key protein in maintaining the integrity of the genome by inducing either cell cycle arrest or apoptosis following cellular stress signals. Two human family members, Mdm2 and Mdmx, are primarily responsible for inactivating p53 transcription and targeting p53 protein for ubiquitin-mediated degradation. In response to genotoxic stress, post-translational modifications to p53, Mdm2 and Mdmx stabilize and activate p53. The role that phosphorylation of these molecules plays in the cellular response to genotoxic agents has been extensively studied with respect to cancer biology. In this review, we discuss the main phosphorylation events of p53, Mdm2 and Mdmx in response to DNA damage that are important for p53 stability and activity. In tumors that harbor wild-type p53, reactivation of p53 by modulating both Mdm2 and Mdmx signaling is well suited as a therapeutic strategy. However, the rationale for development of kinase inhibitors that target the Mdm2-Mdmx-p53 axis must be carefully considered since modulation of certain kinase signaling pathways has the potential to destabilize and inactivate p53.
Identifiers
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.