ArticleThe EMBO journal1997
An alternative pathway for gene regulation by Myc.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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The trial behind it
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Who cites it
161 citing papers in PubMed, 363 citations in OpenAlex.
- MIZ-1 controls transcriptional programs required for BCR signaling, actin dynamics, and naïve B cell survival.Frontiers in immunology · 2026Article
- AlphaFold-Guided Discovery of an Overlapping MYC/Miz-1 Interface Enables Peptidomimetic Disruption of MYC/MAX.ChemMedChem · 2025Article
- Defining the MYC-regulated transcriptome and kinome that support KRAS- and ERK-dependent growth of pancreatic cancer.Science signaling · 2025Article
- Article
- ZBTB17/MIZ1 promotes peroxisome biogenesis by transcriptional regulation of PEX13.The Journal of cell biology · 2025Article
- Chromosome 8q24 amplification associated with human hepatocellular carcinoma predicts MYC/ZEB1/MIZ1 transcriptional regulation.Scientific reports · 2024Article
- Miz1 represses type I interferon production and limits viral clearance during influenza A virus infection.Science signaling · 2024Article
- Regulation of BCR-mediated CaScience immunology · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Targeting MYC induces lipid droplet accumulation by upregulation of HILPDA in clear cell renal cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Suppression of interferon α and γ response by Huwe1-mediated Miz1 degradation promotes SARS-CoV-2 replication.Frontiers in immunology · 2024Article
- MYC disrupts transcriptional and metabolic circadian oscillations in cancer and promotes enhanced biosynthesis.bioRxiv : the preprint server for biology · 2023Article
- MYC disrupts transcriptional and metabolic circadian oscillations in cancer and promotes enhanced biosynthesis.PLoS genetics · 2023Article
- RUNX3 inactivates oncogenic MYC through disruption of MYC/MAX complex and subsequent recruitment of GSK3β-FBXW7 cascade.Communications biology · 2023Article
- Miz1 promotes KRAS-driven lung tumorigenesis by repressing the protocadherin Pcdh10.Cancer letters · 2023Article
- MYC Overexpression Drives Immune Evasion in Hepatocellular Carcinoma That Is Reversible through Restoration of Proinflammatory Macrophages.Cancer research · 2023Article
- Suppression of Allergic Asthma by Loss of Function of Miz1-mediated Th1 Skewing.American journal of respiratory cell and molecular biology · 2022Article
- Myc-Interacting Zinc Finger Protein 1 (Miz-1) Is Essential to Maintain Homeostasis and Immunocompetence of the B Cell Lineage.Biology · 2022Article
- Structures and biological functions of zinc finger proteins and their roles in hepatocellular carcinoma.Biomarker research · 2022Review
- Mechanisms of Binding Specificity among bHLH Transcription Factors.International journal of molecular sciences · 2021Review
101 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Myc protein activates transcription as part of a heteromeric complex with Max. However, Myc-transformed cells are characterized by loss of expression of several genes, suggesting that Myc may also repress gene expression. Two-hybrid cloning identifies a novel POZ domain Zn finger protein (Miz-1; Myc-interacting Zn finger protein-1) that specifically interacts with Myc, but not with Max or USF. Miz-1 binds to start sites of the adenovirus major late and cyclin D1 promoters and activates transcription from both promoters. Miz-1 has a potent growth arrest function. Binding of Myc to Miz-1 requires the helix-loop-helix domain of Myc and a short amphipathic helix located in the carboxy-terminus of Miz-1. Expression of Myc inhibits transactivation, overcomes Miz-1-induced growth arrest and renders Miz-1 insoluble in vivo. These processes depend on Myc and Miz-1 association and on the integrity of the POZ domain of Miz-1, suggesting that Myc binding activates a latent inhibitory function of this domain. Fusion of a nuclear localization signal induces efficient nuclear transport of Miz-1 and impairs the ability of Myc to overcome transcriptional activation and growth arrest by Miz-1. Our data suggest a model for how gene repression by Myc may occur in vivo.
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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.