ArticleProceedings of the National Academy of Sciences of the United States of America2002
Myc and Mad bHLHZ domains possess identical DNA-binding specificities but only partially overlapping functions in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 67 citations in OpenAlex.
- The power of the (imperfect) palindrome: Sequence-specific roles of palindromic motifs in gene regulation.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Review
- Yamanaka Factors in the Budding TunicateFrontiers in cell and developmental biology · 2022Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- A novel SMAD family protein, SMAD9 is involved in follicular initiation and changes egg yield of geese via synonymous mutations in exon1 and intron2.Molecular biology reports · 2015Article
- Genome recognition by MYC.Cold Spring Harbor perspectives in medicine · 2014Review
- Sequence specificity incompletely defines the genome-wide occupancy of Myc.Genome biology · 2014Article
- MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib.Nucleic acids research · 2014Article
- Myc binds the pluripotency factor Utf1 through the basic-helix-loop-helix leucine zipper domain.Biochemical and biophysical research communications · 2013Article
- cMyc/miR-125b-5p signalling determines sensitivity to bortezomib in preclinical model of cutaneous T-cell lymphomas.PloS one · 2013Article
- c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells.Cell · 2012Article
- DNA methylation analyses of urothelial carcinoma reveal distinct epigenetic subtypes and an association between gene copy number and methylation status.Epigenetics · 2012Article
- Review
- Article
- Myc's broad reach.Genes & development · 2008Review
- siRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells.Journal of experimental & clinical cancer research : CR · 2008Article
- Hypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity.Molecular cancer · 2008Article
- Global identification of Myc target genes reveals its direct role in mitochondrial biogenesis and its E-box usage in vivo.PloS one · 2008Article
- Proteomic discovery of Max as a novel interacting partner of C/EBPalpha: a Myc/Max/Mad link.Leukemia · 2006Article
- Assembly of b/HLH/z proteins c-Myc, Max, and Mad1 with cognate DNA: importance of protein-protein and protein-DNA interactions.Biochemistry · 2005Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The opposing transcriptional activities of the basic-helix-loop-helix-leucine zipper proteins Myc and Mad, taken together with information related to their expression patterns and biological effects, have led to a model of the Myc/Max/Mad network in which Myc and Mad proteins function as antagonists. This antagonism is presumed to operate at the level of genes targeted by these complexes, where Myc:Max activates and Mad:Max represses expression of the same set of genes. However, a detailed analysis of the DNA-binding preferences for Mad proteins has not been performed. Furthermore, the model does not address the findings that Myc:Max indirectly represses transcription of several regulatory genes. To examine these issues relating to DNA-binding specificity and biological responses, we have determined the DNA-binding preferences of Mad1 by using selection and amplification of randomized oligonucleotides and demonstrated that its intrinsic specificity is identical with that of c-Myc. We have also used a chimeric Myc protein, containing a substitution of the entire Mad basic-helix-loop-helix-leucine zipper motif, and shown that it can reproduce the growth-promoting activities of Myc, but not its apoptotic function. Our results suggest that Myc and Mad, although possessing identical in vitro DNA-binding specificities, do not have an identical set of target genes in vivo, and that apoptosis is one biological outcome in which the transcriptional effects of Myc are not directly antagonized by those of Mad.
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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.