ArticleACS central science2021
Parallel Automated Flow Synthesis of Covalent Protein Complexes That Can Inhibit MYC-Driven Transcription.
Article in ACS central science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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
15 citing papers in PubMed, 36 citations in OpenAlex.
- Advancing protein engineering via organic chemistry.Communications chemistry · 2026Review
- Article
- Engineering Light-Responsive Transcription Factors via Strategic Masking of Post-translational Modification Residues.Bioconjugate chemistry · 2026Article
- AlphaFold-Guided Discovery of an Overlapping MYC/Miz-1 Interface Enables Peptidomimetic Disruption of MYC/MAX.ChemMedChem · 2025Article
- Chemical Engineering of Transcription Factors Uncovered Cell-Permeable μMax Modulators.Journal of the American Chemical Society · 2025Article
- Advances in the chemical synthesis of human proteoforms.Science China. Life sciences · 2025Review
- Beyond small molecules: advancing MYC-targeted cancer therapies through protein engineering.Transcription · 2025Review
- Development of DuoMYC: a synthetic cell penetrant miniprotein that efficiently inhibits the oncogenic transcription factor MYC.Angewandte Chemie (International ed. in English) · 2025Article
- A Versatile Method for Site-Specific Chemical Installation of Aromatic Posttranslational Modification Analogs into Proteins.Journal of the American Chemical Society · 2024Article
- Site-Specific Acetylation of the Transcription Factor Protein Max Modulates Its DNA Binding Activity.ACS central science · 2024Article
- Automated Flow Peptide Synthesis Enables Engineering of Proteins with Stabilized Transient Binding Pockets.ACS central science · 2024Article
- Enabling Peptide Ligation at Aromatic Junction Mimics via Native Chemical Ligation and Palladium-Mediated S-Arylation.Organic letters · 2023Article
- Branched Multimeric Peptides as Affinity Reagents for the Detection of α-Klotho Protein.Angewandte Chemie (International ed. in English) · 2023Article
- Chemical and Enzymatic Methods for Post-Translational Protein-Protein Conjugation.Journal of the American Chemical Society · 2022Review
- Posttranslational Chemical Mutagenesis Methods to Insert Posttranslational Modifications into Recombinant Proteins.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Dysregulation of the transcription factor MYC is involved in many human cancers. The dimeric transcription factor complexes of MYC/MAX and MAX/MAX activate or inhibit, respectively, gene transcription upon binding to the same enhancer box DNA. Targeting these complexes in cancer is a long-standing challenge. Inspired by the inhibitory activity of the MAX/MAX dimer, we engineered covalently linked, synthetic homo- and heterodimeric protein complexes to attenuate oncogenic MYC-driven transcription. We prepared the covalent protein complexes (∼20 kDa, 167-231 residues) in a single shot via parallel automated flow synthesis in hours. The stabilized covalent dimers display DNA binding activity, are intrinsically cell-penetrant, and inhibit cancer cell proliferation in different cell lines. RNA sequencing and gene set enrichment analysis in A549 cancer cells confirmed that the synthetic dimers interfere with MYC-driven transcription. Our results demonstrate the potential of automated flow technology to rapidly deliver engineered synthetic protein complex mimetics that can serve as a starting point in developing inhibitors of MYC-driven cancer cell growth.
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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.