ArticleNature communications2024
Molecular basis of VEGFR1 autoinhibition at the plasma membrane.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 15 citations in OpenAlex.
- Structure-Activity Relationship Evaluation of Melatonin and Its Derivatives for Wound-Healing Applications: A Combined Network Pharmacology, Molecular Docking, and Biological Validation Approach.International journal of molecular sciences · 2026Article
- Mechanisms of VEGFR2 activation by VEGF, neuropilin, and heparin.Science advances · 2026Article
- Exploring the potential targets and mechanisms of artemisinin in the treatment of diabetic kidney disease using network pharmacology and molecular docking.Functional & integrative genomics · 2026Article
- VEGFR1 as a Target for Cardiovascular Gene Therapy.Journal of cardiovascular translational research · 2025Review
- Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- OPN3-mediated positive regulation of angiogenesis in HUVECs through VEGFR2 interaction.Communications biology · 2025Article
- Exploring structure-function relationships in engineered receptor performance using computational structure prediction.GEN biotechnology · 2025Article
- The use of intuitive AF-based modelling for the understanding of activation and signalling through insulin-like receptors.Frontiers in endocrinology · 2025Review
- Exploring structure-function relationships in engineered receptor performance using computational structure prediction.bioRxiv : the preprint server for biology · 2024Article
- Soluble FLT-1 in angiogenesis: pathophysiological roles and therapeutic implications.Angiogenesis · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ligand-independent activation of VEGFRs is a hallmark of diabetes and several cancers. Like EGFR, VEGFR2 is activated spontaneously at high receptor concentrations. VEGFR1, on the other hand, remains constitutively inactive in the unligated state, making it an exception among VEGFRs. Ligand stimulation transiently phosphorylates VEGFR1 and induces weak kinase activation in endothelial cells. Recent studies, however, suggest that VEGFR1 signaling is indispensable in regulating various physiological or pathological events. The reason why VEGFR1 is regulated differently from other VEGFRs remains unknown. Here, we elucidate a mechanism of juxtamembrane inhibition that shifts the equilibrium of VEGFR1 towards the inactive state, rendering it an inefficient kinase. The juxtamembrane inhibition of VEGFR1 suppresses its basal phosphorylation even at high receptor concentrations and transiently stabilizes tyrosine phosphorylation after ligand stimulation. We conclude that a subtle imbalance in phosphatase activation or removing juxtamembrane inhibition is sufficient to induce ligand-independent activation of VEGFR1 and sustain tyrosine phosphorylation.
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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.