ArticleMolecular and cellular biology2000
Myc is an essential negative regulator of platelet-derived growth factor beta receptor expression.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 63 citations in OpenAlex.
- A circular RNA promotes tumorigenesis by inducing c-myc nuclear translocation.Cell death and differentiation · 2017Article
- ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.Nature communications · 2016Article
- Assessing adaptation of the cancer kinome in response to targeted therapies.Biochemical Society transactions · 2014Review
- p19Arf represses platelet-derived growth factor receptor β by transcriptional and posttranscriptional mechanisms.Molecular and cellular biology · 2012Article
- Article
- Application of autologous derived-platelet rich plasma gel in the treatment of chronic wound ulcer: diabetic foot ulcer.The journal of extra-corporeal technology · 2010Review
- Degradation of activated protein kinases by ubiquitination.Annual review of biochemistry · 2009Review
- Article
- Integration of genome and chromatin structure with gene expression profiles to predict c-MYC recognition site binding and function.PLoS computational biology · 2007Article
- Molecular pathogenesis of chronic wounds: the role of beta-catenin and c-myc in the inhibition of epithelialization and wound healing.The American journal of pathology · 2005Article
- Promoter-binding and repression of PDGFRB by c-Myc are separable activities.Nucleic acids research · 2004Article
- Review
- Article
- Translocations involving c-myc and c-myc function.Oncogene · 2001Review
- Myc potentiates apoptosis by stimulating Bax activity at the mitochondria.Molecular and cellular biology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet-derived growth factor BB (PDGF BB) is a potent mitogen for fibroblasts as well as many other cell types. Interaction of PDGF BB with the PDGF beta receptor (PDGF-betaR) activates numerous signaling pathways and leads to a decrease in receptor expression on the cell surface. PDGF-betaR downregulation is effected at two levels, the immediate internalization of ligand-receptor complexes and the reduction in pdgf-betar mRNA expression. Our studies show that pdgf-betar mRNA suppression is regulated by the c-myc proto-oncogene. Both constitutive and inducible ectopic Myc protein can suppress pdgf-betar mRNA and protein. Suppression of pdgf-betar mRNA in response to Myc is specific, since expression of the related receptor pdgf-alphar is not affected. We further show that Myc suppresses pdgf-betar mRNA expression by a mechanism which is distinguishable from Myc autosuppression. Analysis of c-Myc-null fibroblasts demonstrates that Myc is required for the repression of pdgf-betar mRNA expression in quiescent fibroblasts following mitogen stimulation. In addition, it is evident that the Myc-mediated repression of pdgf-betar mRNA levels plays an important role in the regulation of basal pdgf-betar expression in proliferating cells. Thus, our studies suggest an essential role for Myc in a negative-feedback loop regulating the expression of the PDGF-betaR.
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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.