ArticleMolecular and cellular biology2004
Visualization of Myc/Max/Mad family dimers and the competition for dimerization in living cells.
Article in Molecular and cellular biology, 2004. 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.
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Who cites it
62 citing papers in PubMed, 168 citations in OpenAlex.
- MYC Is Functionally Required in Both Normal and Neoplastic Meibomian Glands.The American journal of pathology · 2026Article
- Beyond small molecules: advancing MYC-targeted cancer therapies through protein engineering.Transcription · 2025Review
- Surprising features of nuclear receptor interaction networks revealed by live-cell single-molecule imaging.eLife · 2025Article
- Surprising Features of Nuclear Receptor Interaction Networks Revealed by Live Cell Single Molecule Imaging.bioRxiv : the preprint server for biology · 2024Article
- A genome-first approach to variants in MLXIPL and their association with hepatic steatosis and plasma lipids.Hepatology communications · 2024Article
- Dual-transgenic BiFC vector systems for protein-protein interaction analysis in plants.Frontiers in genetics · 2024Article
- Laser nanostructured gold biosensor for proto-oncogene detection.Scientific reports · 2023Article
- Liver transcriptomic and methylomic analyses identify transcriptional mitogen-activated protein kinase regulation in facultative hibernation of Syrian hamster.Proceedings. Biological sciences · 2023Article
- Study of the Bcl-2 Interactome by BiFC Reveals Differences in the Activation Mechanism of Bax and Bak.Cells · 2023Article
- Bimolecular Fluorescence Complementation Assay to Evaluate HSP90-Client Protein Interactions in Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Hyperoxia Inhibits Proliferation of Retinal Endothelial Cells in a Myc-Dependent Manner.Life (Basel, Switzerland) · 2021Article
- LACC1 deficiency links juvenile arthritis with autophagy and metabolism in macrophages.The Journal of experimental medicine · 2021Article
- The Molecular 'Myc-anisms' Behind Myc-Driven Tumorigenesis and the Relevant Myc-Directed Therapeutics.International journal of molecular sciences · 2020Review
- Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches.International journal of molecular sciences · 2018Review
- A selective high affinity MYC-binding compound inhibits MYC:MAX interaction and MYC-dependent tumor cell proliferation.Scientific reports · 2018Article
- MAX Mutations in Endometrial Cancer: Clinicopathologic Associations and Recurrent MAX p.His28Arg Functional Characterization.Journal of the National Cancer Institute · 2018Article
- Frontline Science: c-Myc regulates P-selectin glycoprotein ligand-1 expression in monocytes during HIV-1 infection.Journal of leukocyte biology · 2017Article
- c-MYC-Making Liver Sick: Role of c-MYC in Hepatic Cell Function, Homeostasis and Disease.Genes · 2017Review
- Social stress in adolescents induces depression and brain-region-specific modulation of the transcription factor MAX.Translational psychiatry · 2016Article
- In vitro visualization and characterization of wild type and mutant IDH homo- and heterodimers using Bimolecular Fluorescence Complementation.Cancer research frontiers · 2016Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myc and Mad family proteins play opposing roles in the control of cell growth and proliferation. We have visualized the subcellular locations of complexes formed by Myc/Max/Mad family proteins using bimolecular fluorescence complementation (BiFC) analysis. Max was recruited to different subnuclear locations by interactions with Myc versus Mad family members. Complexes formed by Max with Mxi1, Mad3, or Mad4 were enriched in nuclear foci, whereas complexes formed with Myc were more uniformly distributed in the nucleoplasm. Mad4 was localized to the cytoplasm when it was expressed separately, and Mad4 was recruited to the nucleus through dimerization with Max. The cytoplasmic localization of Mad4 was determined by a CRM1-dependent nuclear export signal located near the amino terminus. We compared the relative efficiencies of complex formation among Myc, Max, and Mad family proteins in living cells using multicolor BiFC analysis. Max formed heterodimers with the basic helix-loop-helix leucine zipper (bHLHZIP) domain of Myc (bMyc) more efficiently than it formed homodimers. Replacement of two amino acid residues in the leucine zipper of Max reversed the relative efficiencies of homo- and heterodimerization in cells. Surprisingly, Mad3 formed complexes with Max less efficiently than bMyc, whereas Mad4 formed complexes with Max more efficiently than bMyc. The distinct subcellular locations and the differences between the efficiencies of dimerization with Max indicate that Mad3 and Mad4 are likely to modulate transcription activation by Myc at least in part through distinct mechanisms.
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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.