ArticleMolecular and cellular biology1998
The promyelocytic leukemia protein interacts with Sp1 and inhibits its transactivation of the epidermal growth factor receptor promoter.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 123 citations in OpenAlex.
- Apoptotic vesicles from endothelial cells promote endothelial progenitor cell differentiation and angiogenesis via miR-30a-5p mediated activation of the EGFR/PI3K/AKT/VEGF pathway.Stem cell research & therapy · 2026Article
- Review
- Discovery and validation of information theory-based transcription factor and cofactor binding site motifs.Nucleic acids research · 2017Article
- Identification of epigenetic signature associated with alpha thalassemia/mental retardation X-linked syndrome.Epigenetics & chromatin · 2017Article
- Role of ND10 nuclear bodies in the chromatin repression of HSV-1.Virology journal · 2016Review
- The function, regulation and therapeutic implications of the tumor suppressor protein, PML.Cell & bioscience · 2015Review
- PML-mediated signaling and its role in cancer stem cells.Oncogene · 2014Review
- Article
- The adenoviral oncogene E1A-13S interacts with a specific isoform of the tumor suppressor PML to enhance viral transcription.Journal of virology · 2013Article
- Nuclear domain 10-associated proteins recognize and segregate intranuclear DNA/protein complexes to negate gene expression.Virology journal · 2012Article
- In vivo regulation of the heme oxygenase-1 gene in humanized transgenic mice.Kidney international · 2012Article
- Promoters of cancer genes for recombinant protein expression in human cancer cell lines.BioImpacts : BI · 2012Article
- The promyelocytic leukemia zinc finger protein: two decades of molecular oncology.Frontiers in oncology · 2012Article
- Promyelocytic leukemia protein in retinoic acid-induced chromatin remodeling of Oct4 gene promoter.Stem cells (Dayton, Ohio) · 2011Article
- Article
- PML involvement in the p73-mediated E1A-induced suppression of EGFR and induction of apoptosis in head and neck cancers.Oncogene · 2009Article
- Signal-dependent regulation of transcription by histone deacetylase 7 involves recruitment to promyelocytic leukemia protein nuclear bodies.Molecular biology of the cell · 2008Article
- p400 function is required for the adenovirus E1A-mediated suppression of EGFR and tumour cell killing.Oncogene · 2007Article
- Transcriptional regulation is affected by subnuclear targeting of reporter plasmids to PML nuclear bodies.Molecular and cellular biology · 2006Article
- Sp2 localizes to subnuclear foci associated with the nuclear matrix.Molecular biology of the cell · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The promyelocytic leukemia protein (PML) is a nuclear phosphoprotein with growth- and transformation-suppressing ability. Having previously shown it to be a transcriptional repressor of the epidermal growth factor receptor (EGFR) gene promoter, we have now shown that PML's repression of EGFR transcription is caused by inhibition of EGFR's Sp1-dependent activity. On functional analysis, the repressive effect of PML was mapped to a 150-bp element (the sequences between -150 and -16, relative to the ATG initiation site) of the promoter. Transient transfection assays with Sp1-negative Drosophila melanogaster SL2 cells showed that the transcription of this region was regulated by Sp1 and that the Sp1-dependent activity of the promoter was suppressed by PML in a dose-dependent manner. Coimmunoprecipitation and mammalian two-hybrid assays demonstrated that PML and Sp1 were associated in vivo. In vitro binding by means of the glutathione S-transferase (GST) pull-down assay, using the full-length and truncated GST-Sp1 proteins and in vitro-translated PML, showed that PML and Sp1 directly interacted and that the C-terminal (DNA-binding) region of Sp1 and the coiled-coil (dimerization) domain of PML were essential for this interaction. Analysis of the effects of PML on Sp1 DNA binding by electrophoretic mobility shift assay (EMSA) showed that PML could specifically disrupt the binding of Sp1 to DNA. Furthermore, cotransfection of PML specifically repressed Sp1, but not the E2F1-mediated activity of the dihydrofolate reductase promoter. Together, these data suggest that the association of PML and Sp1 represents a novel mechanism for negative regulation of EGFR and other Sp1 target promoters.
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.