ArticleMolecular and cellular biology2007
A single-nucleotide polymorphism in a half-binding site creates p53 and estrogen receptor control of vascular endothelial growth factor receptor 1.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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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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
42 citing papers in PubMed, 67 citations in OpenAlex.
- VEGFR1 as a Target for Cardiovascular Gene Therapy.Journal of cardiovascular translational research · 2025Review
- p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiated luminal identity in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Review
- Shared gene targets of the ATF4 and p53 transcriptional networks.bioRxiv : the preprint server for biology · 2023Article
- Shared Gene Targets of the ATF4 and p53 Transcriptional Networks.Molecular and cellular biology · 2023Article
- Article
- The complex architecture of p53 binding sites.Nucleic acids research · 2021Article
- Making Connections: p53 and the Cathepsin Proteases as Co-Regulators of Cancer and Apoptosis.Cancers · 2020Review
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- Influence of Estrogens on Uterine Vascular Adaptation in Normal and Preeclamptic Pregnancies.International journal of molecular sciences · 2020Review
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- FLT1 and transcriptome-wide polyadenylation site (PAS) analysis in preeclampsia.Scientific reports · 2017Article
- Mitochondrial stress-induced p53 attenuates HIF-1α activity by physical association and enhanced ubiquitination.Oncogene · 2017Article
- A/T gap tolerance in the core sequence and flanking sequence requirements of non-canonical p53 response elements.Journal of biochemistry · 2016Article
- Identification of a Functional Risk Variant for Pemphigus Vulgaris in the ST18 Gene.PLoS genetics · 2016Article
- Whole-genome cartography of p53 response elements ranked on transactivation potential.BMC genomics · 2015Article
- Association of VEGF and VEGFR1 polymorphisms with breast cancer risk in North Indians.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Epistatic interaction of Arg72Pro TP53 and -710 C/T VEGFR1 polymorphisms in breast cancer: predisposition and survival.Molecular and cellular biochemistry · 2013Article
- Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Interactions between master regulatory pathways provide higher-order controls for cellular regulation. Recently, we reported a C-->T single-nucleotide polymorphism (SNP) in the vascular endothelial growth factor receptor 1 (VEGFR-1/Flt1) promoter that merges human VEGF and p53 pathways. This finding suggested a new layer in environmental controls of a pathway relevant to several diseases. The Flt1-T SNP created what appeared to be a half-site p53 target response element (RE). The absence of information about p53 gene responsiveness mediated by half-site REs led us to address how it influences Flt1 expression. We now identify a second regulatory sequence comprising a partial RE for estrogen receptors (ERs) upstream of the p53 binding site. Surprisingly, this provides for synergistic stimulation of transcription specifically at the Flt1-T allele through the combined action of ligand-bound ER and stress-induced p53. In addition to demonstrating direct control of Flt1 expression by ER and p53 proteins acting as sequence-specific transcription factors at half-site REs, we establish a new interaction between three master regulatory pathways, p53, ER, and VEGF. The mechanism of joint regulation through half-sites is likely relevant to transcriptional control of other targets and expands the number of genes that may be directly controlled in master regulatory networks.
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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.