ArticleThe EMBO journal1995
Transcriptional activation by Myc is under negative control by the transcription factor AP-2.
Article in The EMBO journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 199 citations in OpenAlex.
- Mammalian Proteome Profiling Reveals Readers and Antireaders of Strand-Symmetric and -Asymmetric 5-Hydroxymethylcytosine-Modifications in DNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fibroblast exosomal TFAP2C induced by chitosan oligosaccharides promotes peripheral axon regeneration via the miR-132-5p/CAMKK1 axis.Bioactive materials · 2023Article
- GRHL2 and AP2a coordinate early surface ectoderm lineage commitment during development.iScience · 2023Article
- Isotretinoin and Thalidomide Down-RegulateMolecules (Basel, Switzerland) · 2021Article
- MYC dysfunction modulates stemness and tumorigenesis in breast cancer.International journal of biological sciences · 2021Article
- The functions and mechanisms of prefoldin complex and prefoldin-subunits.Cell & bioscience · 2020Review
- Dysregulated Transcription Factor TFAP2A After Peripheral Nerve Injury Modulated Schwann Cell Phenotype.Neurochemical research · 2019Article
- A human specific Alu DNA cassette is found flanking the genes of transcription factor AP2.BMC research notes · 2019Article
- Tuberous sclerosis complex is required for tumor maintenance in MYC-driven Burkitt's lymphoma.The EMBO journal · 2018Article
- Genetic Dissection of a Supergene ImplicatesGenetics · 2018Article
- Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas.Acta neuropathologica communications · 2017Article
- Article
- Transcription factor activating protein 2 beta (TFAP2B) mediates noradrenergic neuronal differentiation in neuroblastoma.Molecular oncology · 2016Article
- Identification of the β-catenin/JNK/prothymosin-alpha axis as a novel target of sorafenib in hepatocellular carcinoma cells.Oncotarget · 2015Article
- MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.Oncotarget · 2015Article
- Article
- Small-molecule inhibitors of the Myc oncoprotein.Biochimica et biophysica acta · 2015Review
- Long-range enhancers regulating Myc expression are required for normal facial morphogenesis.Nature genetics · 2014Article
- Association of the human astrocyte elevated gene-1 promoter variants with susceptibility to hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2014Article
- Calcium efflux activity of plasma membrane Ca2+ ATPase-4 (PMCA4) mediates cell cycle progression in vascular smooth muscle cells.The Journal of biological chemistry · 2014Article
15 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Myc protein binds to and transactivates the expression of genes via E-box elements containing a central CAC(G/A)TG sequence. The transcriptional activation function of Myc is required for its ability to induce cell cycle progression, cellular transformation and apoptosis. Here we show that transactivation by Myc is under negative control by the transcription factor AP-2. AP-2 inhibits transactivation by Myc via two distinct mechanisms. First, high affinity binding sites for AP-2 overlap Myc-response elements in two bona fide target genes of Myc, prothymosin-alpha and ornithine decarboxylase. On these sites, AP-2 competes for binding of either Myc/Max heterodimers or Max/Max homodimers. The second mechanism involves a specific interaction between C-terminal domains of AP-2 and the BR/HLH/LZ domain of Myc, but not Max or Mad. Binding of AP-2 to Myc does not preclude association of Myc with Max, but impairs DNA binding of the Myc/Max complex and inhibits transactivation by Myc even in the absence of an overlapping AP-2 binding site. Taken together, our data suggest that AP-2 acts as a negative regulator of transactivation by Myc.
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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.