ArticleBritish journal of pharmacology2015
Effects of receptor tyrosine kinase inhibitors on VEGF165 a- and VEGF165 b-stimulated gene transcription in HEK-293 cells expressing human VEGFR2.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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, 13 citations in OpenAlex.
- The VEGF/VEGFR Axis Revisited: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- Comparison of the ligand-binding properties of fluorescent VEGF-A isoforms to VEGF receptor 2 in living cells and membrane preparations using NanoBRET.British journal of pharmacology · 2019Article
- Complex Formation between VEGFR2 and the βCell chemical biology · 2019Article
- Long-term cardiovascular effects of vandetanib and pazopanib in normotensive rats.Pharmacology research & perspectives · 2019Article
- Utilizing a Simple Method for Stoichiometric Protein Labeling to Quantify Antibody Blockade.Scientific reports · 2019Article
- Real-Time Ligand Binding of Fluorescent VEGF-A Isoforms that Discriminate between VEGFR2 and NRP1 in Living Cells.Cell chemical biology · 2018Article
- Real-time analysis of the binding of fluorescent VEGFBiochemical pharmacology · 2017Article
- Effects of 4 multitargeted receptor tyrosine kinase inhibitors on regional hemodynamics in conscious, freely moving rats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Pro- and antiangiogenic VEGF and its receptor status for the severity of diabetic retinopathy.Molecular vision · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeReceptor tyrosine kinase inhibitors (RTKIs) targeted at VEGF receptor 2 (VEGFR2) have proved to be attractive approaches to cancer therapy based on their ability to reduce angiogenesis. Here we have undertaken a quantitative analysis of the interaction of RTKIs and two VEGF splice variants, VEGF(165)a and VEGF(165)b, with VEGFR2 by studying nuclear factor of activated T-cells (NFAT) reporter gene activity in live HEK-293 cells. EXPERIMENTAL APPROACH: HEK-293 cells expressing the human VEGFR2 and a firefly luciferase reporter gene regulated by an NFAT response element were used for quantitative analysis of the effect of RTKIs on VEGF(165)a- and VEGF(165)b-stimulated luciferase gene expression. KEY
resultsVEGF(165)a produced a concentration-dependent activation of the NFAT-luciferase reporter gene in living cells that was inhibited in a non-competitive fashion by four different RTKIs (cediranib, pazopanib, sorafenib and vandetanib). The potency obtained for each RTKI from this analysis was similar to those obtained in binding studies using purified VEGFR2 kinase domains. VEGF(165)b was a lower-efficacy agonist of the NFAT-luciferase response when compared with VEGF(165)a. Analysis of the concentration-response data using the operational model of agonism indicated that both VEGF(165) isoforms had similar affinity for VEGFR2. CONCLUSIONS AND IMPLICATIONS: Quantitative pharmacological analysis of the interaction of VEGF(165) isoforms and RTKIs with VEGFR2 in intact living cells has provided important insights into the relative affinity and efficacy of VEGF(165)a and VEGF(165)b for activation of the calcineurin- NFAT signalling pathway by this tyrosine kinase receptor.
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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.