ArticleThe Journal of clinical investigation1996
A link between c-Myc-mediated transcriptional repression and neoplastic transformation.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 68 citations in OpenAlex.
- Regulation of the somatotropic axis by MYC-mediated miRNA repression.Frontiers in cell and developmental biology · 2023Article
- Review
- Article
- Co-overexpression of bcl-2 and c-myc in uterine cervix carcinomas and premalignant lesions.European journal of histochemistry : EJH · 2011Article
- Emerging Concepts in the Analysis of Transcriptional Targets of the MYC Oncoprotein: Are the Targets Targetable?Genes & cancer · 2010Article
- Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assays.BMC biochemistry · 2005Article
- Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases.World journal of gastroenterology · 2004Article
- c-Myc represses the proximal promoters of GADD45a and GADD153 by a post-RNA polymerase II recruitment mechanism.Oncogene · 2004Article
- Article
- Cell cycle arrest and repression of cyclin D1 transcription by INI1/hSNF5.Molecular and cellular biology · 2002Article
- N-myc oncogene overexpression down-regulates IL-6; evidence that IL-6 inhibits angiogenesis and suppresses neuroblastoma tumor growth.Oncogene · 2002Article
- Reconstitution of hTERT restores tumorigenicity in melanoma-derived c-Myc low-expressing clones.Oncogene · 2002Article
- Article
- Translocations involving c-myc and c-myc function.Oncogene · 2001Review
- Myc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Repression of transcription of the p27(Kip1) cyclin-dependent kinase inhibitor gene by c-Myc.Oncogene · 2001Article
- Transforming ability of Gag-Myc fusion proteins correlates with Gag-Myc protein stability and transcriptional repression.Oncogene · 2001Article
- Myc is an essential negative regulator of platelet-derived growth factor beta receptor expression.Molecular and cellular biology · 2000Article
- Induction of cell cycle progression and acceleration of apoptosis are two separable functions of c-Myc: transrepression correlates with acceleration of apoptosis.Molecular and cellular biology · 2000Article
- Mechanisms of apoptosis by c-Myc.Oncogene · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies indicate that the transcription factor c-Myc contributes to oncogenesis by altering the expression of genes involved in cell proliferation, but its precise function in neoplasia remains ambiguous. The ability of c-Myc to bind the sequence CAC(G/A)TG and transactivate appears to be linked to its transforming activity; however, c-Myc also represses transcription in vitro through a pyrimidine-rich cis element termed the initiator (Inr). In transfection experiments using the adenoviral major late (adML) promoter, which contains two Myc binding sites and an Inr, we determined that c-Myc represses transcription through the initiator in vivo. This activity requires the dimerization domain and amino acids 106 to 143, which are located within the transactivation domain and are necessary for neoplastic transformation. We studied a lymphoma-derived c-Myc substitution mutation at 115-Phe, which is within the region required for transcriptional suppression, and found the mutant more effective than wild-type c-Myc in transforming rodent fibroblasts and in suppressing the adML promoter. Our studies of both loss-of-function and gain-of-function c-Myc mutations suggest a link between c-Myc-mediated neoplastic transformation and transcriptional repression through the Inr.
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What OpenQuestion holds
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.