ArticleNature structural & molecular biology2017
Structural analysis of MDM2 RING separates degradation from regulation of p53 transcription activity.
Article in Nature structural & molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
- MST4 plays dual roles in lung adenocarcinoma by regulating homeostasis of wild-type and mutant p53 protein.Oncogene · 2026Article
- MDM4 at the Crossroads: Beyond p53 and MDM2.Cancers · 2026Review
- Ubiquitination of MEIS1 by MDM2 serves as a switch for p53 stabilization and DNA damage response activation.Cell death and differentiation · 2026Article
- UBA6 specificity for ubiquitin E2 conjugating enzymes reveals a priority mechanism of BIRC6.Nature structural & molecular biology · 2026Article
- Tuning ubiquitin transfer by RING E3 ubiquitin ligases through the linchpin residue.Life science alliance · 2025Article
- Targeting MDM2 homodimer and heterodimer disruption with DRx-098D inMolecular therapy. Oncology · 2025Article
- Structure and function of MDM2 and MDM4 in health and disease.The Biochemical journal · 2025Review
- MDM2 functions as a timer reporting the length of mitosis.Nature cell biology · 2025Article
- Chemical Tools for Probing the Ub/Ubl Conjugation Cascades.Chembiochem : a European journal of chemical biology · 2025Review
- Multisite phosphorylation dictates selective E2-E3 pairing as revealed by Ubc8/UBE2H-GID/CTLH assemblies.Molecular cell · 2024Article
- Cullin7 induces docetaxel resistance by regulating the protein level of the antiapoptotic protein Survivin in lung adenocarcinoma cells.Journal of thoracic disease · 2023Article
- MDM2 promotes cancer cell survival through regulating the expression of HIF-1α and pVHL in retinoblastoma.Pathology oncology research : POR · 2023Article
- Elucidation of TRIM25 ubiquitination targets involved in diverse cellular and antiviral processes.PLoS pathogens · 2022Article
- Understanding the interaction of 14-3-3 proteins with hDMX and hDM2: a structural and biophysical study.The FEBS journal · 2022Article
- Bivalent binding of p14ARF to MDM2 RING and acidic domains inhibits E3 ligase function.Life science alliance · 2022Article
- Structural studies of antitumor compounds that target the RING domain of MDM2.Protein science : a publication of the Protein Society · 2022Article
- Alterations of the Mdm2 C-Terminus Differentially Impact Its Function In Vivo.Cancer research · 2022Article
- Repressed miR-34a Expression Dictates the Cell Fate to Corneal Endothelium Failure.Investigative ophthalmology & visual science · 2022Article
- Targeted Degradation of 53BP1 Using Ubiquitin Variant Induced Proximity.Biomolecules · 2022Article
- MDMX is essential for the regulation of p53 protein levels in the absence of a functional MDM2 C-terminal tail.BMC molecular and cell biology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
MDM2-MDMX complexes bind the p53 tumor-suppressor protein, inhibiting p53's transcriptional activity and targeting p53 for proteasomal degradation. Inhibitors that disrupt binding between p53 and MDM2 efficiently activate a p53 response, but their use in the treatment of cancers that retain wild-type p53 may be limited by on-target toxicities due to p53 activation in normal tissue. Guided by a novel crystal structure of the MDM2-MDMX-E2(UbcH5B)-ubiquitin complex, we designed MDM2 mutants that prevent E2-ubiquitin binding without altering the RING-domain structure. These mutants lack MDM2's E3 activity but retain the ability to limit p53's transcriptional activity and allow cell proliferation. Cells expressing these mutants respond more quickly to cellular stress than cells expressing wild-type MDM2, but basal p53 control is maintained. Targeting the MDM2 E3-ligase activity could therefore widen the therapeutic window of p53 activation in tumors.
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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.