ArticleNucleic acids research2004
Promoter-binding and repression of PDGFRB by c-Myc are separable activities.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed.
- Transcriptome analysis reveals microvascular endothelial cell-dependent pericyte differentiation.Scientific reports · 2019Article
- Blockade of PDGFRβ circumvents resistance to MEK-JAK inhibition via intratumoral CD8Journal of experimental & clinical cancer research : CR · 2019Article
- Human Cancer Cells Signal Their Competitive Fitness Through MYC Activity.Scientific reports · 2017Article
- p19Arf represses platelet-derived growth factor receptor β by transcriptional and posttranscriptional mechanisms.Molecular and cellular biology · 2012Article
- Article
- A core MYC gene expression signature is prominent in basal-like breast cancer but only partially overlaps the core serum response.PloS one · 2009Article
- Su(z)2 antagonizes auto-repression of Myc in Drosophila, increasing Myc levels and subsequent trans-activation.PloS one · 2009Article
- Coordinated regulation of Myc trans-activation targets by Polycomb and the Trithorax group protein Ash1.BMC molecular biology · 2007Article
- In silico identification of transcriptional regulators associated with c-Myc.Nucleic acids research · 2004Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Myc transcription factor represses the mRNA expression of the platelet-derived growth factor receptor beta gene (PDGFRB). Using chromatin immunoprecipitation, we show that c-Myc binds to the proximal promoter of the PDGFRB gene in proliferating rat fibroblasts. Interestingly, mutant c-Myc proteins that are unable to repress PDGFRB gene expression, c-Myc(dBR) and c-Myc(d106-143), are still able to bind to the promoter in vivo. Hence, promoter-binding and repression of PDGFRB by c-Myc are separable activities. We also show that Myc repression of PDGFRB is not dependent on previously described or known transactivator-binding regions, suggesting Myc may be recruited to the promoter by multiple or yet unidentified transcription factors. In the presence of intact promoter-binding by Myc, trichostatin A (TSA) can block Myc repression of PDGFRB in vivo, again demonstrating that promoter-binding and repression are separable. Taken together, we hypothesize that Myc repression of PDGFRB expression occurs by a multi-step mechanism in which repression is initiated after Myc is recruited to the promoter.
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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.