ArticleProceedings of the National Academy of Sciences of the United States of America1994
Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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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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
46 citing papers in PubMed, 124 citations in OpenAlex.
- MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues.Science advances · 2025Article
- The C. elegans Myc-family of transcription factors coordinate a dynamic adaptive response to dietary restriction.GeroScience · 2024Article
- Mapping chromatin accessibility and active regulatory elements reveals pathological mechanisms in human gliomas.Nature communications · 2021Article
- The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.Frontiers of medicine · 2018Review
- Article
- Diet-induced weight loss leads to a switch in gene regulatory network control in the rectal mucosa.Genomics · 2016Article
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- Article
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
- Cucurbitacin B, a novel in vivo potentiator of gemcitabine with low toxicity in the treatment of pancreatic cancer.British journal of pharmacology · 2010Article
- Activation of PI3K/Akt and MAPK pathways regulates Myc-mediated transcription by phosphorylating and promoting the degradation of Mad1.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Regulation of the MAD1 promoter by G-CSF.Nucleic acids research · 2008Article
- The transcriptional repressor dMnt is a regulator of growth in Drosophila melanogaster.Molecular and cellular biology · 2005Article
- Visualization of Myc/Max/Mad family dimers and the competition for dimerization in living cells.Molecular and cellular biology · 2004Article
- Functional analysis of the Mad1-mSin3A repressor-corepressor interaction reveals determinants of specificity, affinity, and transcriptional response.Molecular and cellular biology · 2004Article
- Review
- Article
- S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells.The Biochemical journal · 2001Article
- Translocations involving c-myc and c-myc function.Oncogene · 2001Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mad and Mxi1, two members of the Myc-related basic-region helix-loop-helix/leucine-zipper family of proteins, associate directly with Max to form sequence-specific DNA binding heterodimers that are transactivation-incompetent. Mad-Max complexes have been shown to exert a strong repressive effect on Myc-induced transactivation, perhaps through the competitive occupation of common promoter binding sites also recognized by active Myc-Max heterodimers. To place these recent biochemical observations in a biological context, mad and mxi1 expression vectors were tested for their ability to influence Myc transformation activity in the rat embryo fibroblast cooperation assay. Addition of an equimolar amount of mad or mxi1 expression vector to mouse c-myc/ras cotransfections resulted in a dramatic reduction in both the number of foci generated and the severity of the malignant phenotype. Myc-specific suppression by Mad and Mxi1 was demonstrated by their ability to affect c- and N-myc-, but not ela-, induced transformation. In contrast, mad and mxi1 expression constructs bearing deletions in the basic region exerted only mild repressive effects on Myc transformation activity, suggesting that occupation of common DNA binding sites by transactivation-incompetent Mad-Max or Mxi1-Max complexes appears to play a more dominant role in this suppression than titration of limited intracellular pools of Max away from active Myc-Max complexes. Thus, these biological data support a current model for regulation of Myc function in which relative intracellular levels of Mad and Mxi1 in comparison to those of Myc may determine the degree of activation of Myc-responsive growth pathways.
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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.