ArticleMolecular pharmacology2009
Stabilizers of the Max homodimer identified in virtual ligand screening inhibit Myc function.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Targeting protein synthesis pathways in MYC-amplified medulloblastoma.Discover oncology · 2025Review
- Article
- Antitumor Effect of Anti-c-Myc Aptamer-Based PROTAC for Degradation of the c-Myc Protein.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Recent advances in targeting the "undruggable" proteins: from drug discovery to clinical trials.Signal transduction and targeted therapy · 2023Review
- Comparative analysis of compound NSC13728 as Omomyc homodimer stabilizer by molecular dynamics simulation and MM/GBSA free energy calculation.Journal of molecular modeling · 2022Article
- Review
- The long journey to bring a Myc inhibitor to the clinic.The Journal of cell biology · 2021Review
- Targeted degradation of transcription factors by TRAFTACs: TRAnscription Factor TArgeting Chimeras.Cell chemical biology · 2021Article
- Taking the Myc out of cancer: toward therapeutic strategies to directly inhibit c-Myc.Molecular cancer · 2021Review
- Transcription Factor Inhibition: Lessons Learned and Emerging Targets.Trends in molecular medicine · 2020Review
- Article
- Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches.International journal of molecular sciences · 2018Review
- The non-enzymatic RAS effector RASSF7 inhibits oncogenic c-Myc function.The Journal of biological chemistry · 2018Article
- Evolution of In Silico Strategies for Protein-Protein Interaction Drug Discovery.Molecules (Basel, Switzerland) · 2018Review
- Strategies to Inhibit Myc and Their Clinical Applicability.Frontiers in cell and developmental biology · 2017Review
- Computational protein-ligand docking and virtual drug screening with the AutoDock suite.Nature protocols · 2016Article
- microRNA-206 impairs c-Myc-driven cancer in a synthetic lethal manner by directly inhibiting MAP3K13.Oncotarget · 2016Article
- MicroRNA-based screens for synthetic lethal interactions with c-Myc.RNA & disease (Houston, Tex.) · 2016Article
- Direct inhibition of c-Myc-Max heterodimers by celastrol and celastrol-inspired triterpenoids.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Many human cancers show constitutive or amplified expression of the transcriptional regulator and oncoprotein Myc, making Myc a potential target for therapeutic intervention. Here we report the down-regulation of Myc activity by reducing the availability of Max, the essential dimerization partner of Myc. Max is expressed constitutively and can form unstable homodimers. We have isolated stabilizers of the Max homodimer by applying virtual ligand screening (VLS) to identify specific binding pockets for small molecule interactors. Candidate compounds found by VLS were screened by fluorescence resonance energy transfer, and from these screens emerged a potent, specific stabilizer of the Max homodimer. In vitro binding assays demonstrated that the stabilizer enhances the formation of the Max-Max homodimer and interferes with the heterodimerization of Myc and Max in a dose-dependent manner. Furthermore, this compound interferes with Myc-induced oncogenic transformation, Myc-dependent cell growth, and Myc-mediated transcriptional activation. The Max-Max stabilizer can be considered a lead compound for the development of inhibitors of the Myc network.
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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.