ArticleBiochemistry2010
Molecular cloning of the human platelet-derived growth factor receptor beta (PDGFR-beta) promoter and drug targeting of the G-quadruplex-forming region to repress PDGFR-beta expression.
Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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
47 citing papers in PubMed, 76 citations in OpenAlex.
- Structures and dynamics of the major G-quadruplex in the human PDGFR-β gene promoter: insights into vacancy G-quadruplex formation.Nucleic acids research · 2026Article
- Article
- Sequence Determinants of G-Quadruplex Thermostability: Aligning Evidence from High-Precision Biophysics and High-Throughput Genomics.Biomolecules · 2025Review
- DNA G-Quadruplexes as Targets for Natural Product Drug Discovery.Engineering (Beijing, China) · 2024Article
- An Engineered Adeno-Associated Virus Capsid Mediates Efficient Transduction of Pericytes and Smooth Muscle Cells of the Brain Vasculature.Human gene therapy · 2023Article
- DNA G-Quadruplex in Human Telomeres and Oncogene Promoters: Structures, Functions, and Small Molecule Targeting.Accounts of chemical research · 2022Article
- High-throughput techniques enable advances in the roles of DNA and RNA secondary structures in transcriptional and post-transcriptional gene regulation.Genome biology · 2022Review
- G-Quadruplex-Binding Proteins: Promising Targets for Drug Design.Biomolecules · 2022Review
- Regulation of PDGFR-β gene expression by targeting the G-vacancy bearing G-quadruplex in promoter.Nucleic acids research · 2021Article
- Solution Structure of Ternary Complex of Berberine Bound to a dGMP-Fill-In Vacancy G-Quadruplex Formed in the PDGFR-β Promoter.Journal of the American Chemical Society · 2021Article
- Chemical targeting of G-quadruplexes in telomeres and beyond for molecular cancer therapeutics.The Journal of antibiotics · 2021Review
- The G4 Resolvase DHX36 Possesses a Prognosis Significance and Exerts Tumour Suppressing Function Through Multiple Causal Regulations in Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Article
- Custom G4 Microarrays Reveal Selective G-Quadruplex Recognition of Small Molecule BMVC: A Large-Scale Assessment of Ligand Binding Selectivity.Molecules (Basel, Switzerland) · 2020Article
- PDGFR-β Promoter Forms a Vacancy G-Quadruplex that Can Be Filled in by dGMP: Solution Structure and Molecular Recognition of Guanine Metabolites and Drugs.Journal of the American Chemical Society · 2020Article
- Review
- Promise of G-Quadruplex Structure Binding Ligands as Epigenetic Modifiers with Anti-Cancer Effects.Molecules (Basel, Switzerland) · 2019Review
- G-Quadruplex DNA and RNA.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Alternative DNA secondary structure formation affects RNA polymerase II promoter-proximal pausing in human.Genome biology · 2018Article
- The 3'-end region of the human PDGFR-β core promoter nuclease hypersensitive element forms a mixture of two unique end-insertion G-quadruplexes.Biochimica et biophysica acta. General subjects · 2018Article
- Mixed guanine, adenine base quartets: possible roles of protons and metal ions in their stabilization.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
To understand the mechanisms controlling platelet-derived growth factor receptor beta (PDGFR-beta) expression in malignancies, we have cloned and characterized the first functional promoter of the human PDGFR-beta gene, which has been confirmed by luciferase reporter gene assays. The transcription initiation sites were mapped by primer extension. Promoter deletion experiments demonstrate that the proximal, highly GC-rich region (positions -165 to -139) of the human PDGFR-beta promoter is crucial for basal promoter activity. This region is sensitive to S1 nuclease and likely to assume a non-B-form DNA secondary structure within the supercoiled plasmid. The G-rich strand in this region contains a series of runs of three or more guanines that can form multiple different G-quadruplex structures, which have been subsequently assessed by circular dichroism. A Taq polymerase stop assay has shown that three different G-quadruplex-interactive drugs can each selectively stabilize different G-quadruplex structures of the human PDGFR-beta promoter. However, in transfection experiments, only telomestatin significantly reduced the human PDGFR-beta basal promoter activity relative to the control. Furthermore, the PDGFR-beta mRNA level in Daoy cells was significantly decreased after treatment with 1 muM telomestatin for 24 h. Therefore, we propose that ligand-mediated stabilization of specific G-quadruplex structures in the human PDGFR-beta promoter can modulate its transcription.
Indexed as
Identifiers
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.