ArticleBlood2011
Regulation of vascular endothelial growth factor receptor 2 trafficking and angiogenesis by Golgi localized t-SNARE syntaxin 6.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Meta-analysis of matrix metalloproteinase (MMP)-9 C1562T polymorphism and susceptibility to ischemic stroke in the Chinese population.The Journal of international medical research · 2020Pooled it
- Oleanolic acid inhibits diet-induced adiposity through blocking neovascularization and macrophage accumulation involving Delta-like 4-Notch 1-nuclear factor-κB signaling.Nutrition research and practice · 2026Article
- A role for theMolecular biology of the cell · 2026Article
- SNARE proteins as biomarkers and therapeutic targets in central nervous system tumors.Discover oncology · 2026Review
- Organelle regulation of SUMOylation: regulatory mechanisms and therapeutic application.Journal of advanced research · 2026Review
- Protein Kinase D Regulates Kinesin-Mediated VEGFR2 Trafficking and Influences Retinal Endothelial Permeability.Traffic (Copenhagen, Denmark) · 2026Article
- Cycling molecular assemblies for Golgi imaging and disruption.Nature communications · 2026Article
- Endocytic Pathways and Actin Remodeling Mediate Everolimus-Induced VE-Cadherin Disorganization and Barrier Dysfunction.Cellular and molecular bioengineering · 2025Article
- A role for thebioRxiv : the preprint server for biology · 2025Article
- Mechanistic computational modeling of sFLT1 secretion dynamics.PLoS computational biology · 2025Article
- The perspective of ceRNA regulation of circadian rhythm on choroidal neovascularization.Scientific reports · 2024Article
- The tyrosine kinase KDR is essential for the survival of HTLV-1-infected T cells by stabilizing the Tax oncoprotein.Nature communications · 2024Article
- A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.Angiogenesis · 2024Article
- The role of syntaxins in retinal function and health.Frontiers in cellular neuroscience · 2024Review
- Article
- KIF13B mediates VEGFR2 recycling to modulate vascular permeability.Cellular and molecular life sciences : CMLS · 2023Article
- A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.bioRxiv : the preprint server for biology · 2023Article
- Syntaxin-6, a Reliable Biomarker for Predicting the Prognosis of Patients with Cancer and the Effectiveness of Immunotherapy.Cancers · 2022Article
- Human Cytomegalovirus Manipulates Syntaxin 6 for Successful Trafficking and Subsequent Infection of Monocytes.Journal of virology · 2022Article
- βNature communications · 2022Article
10 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor receptor 2 (VEGFR2) plays a key role in physiologic and pathologic angiogenesis. Plasma membrane (PM) levels of VEGFR2 are regulated by endocytosis and secretory transport through the Golgi apparatus. To date, the mechanism whereby the VEGFR2 traffics through the Golgi apparatus remains incompletely characterized. We show in human endothelial cells that binding of VEGF to the cell surface localized VEGFR2 stimulates exit of intracellular VEGFR2 from the Golgi apparatus. Brefeldin A treatment reduced the level of surface VEGFR2, confirming that VEGFR2 traffics through the Golgi apparatus en route to the PM. Mechanistically, we show that inhibition of syntaxin 6, a Golgi-localized target membrane-soluble N-ethylmaleimide attachment protein receptor (t-SNARE) protein, interferes with VEGFR2 trafficking to the PM and facilitates lysosomal degradation of the VEGFR2. In cell culture, inhibition of syntaxin 6 also reduced VEGF-induced cell proliferation, cell migration, and vascular tube formation. Furthermore, in a mouse ear model of angiogenesis, an inhibitory form of syntaxin 6 reduced VEGF-induced neovascularization and permeability. Our data demonstrate the importance of syntaxin 6 in the maintenance of cellular VEGFR2 levels, and suggest that the inhibitory form of syntaxin 6 has good potential as an antiangiogenic agent.
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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.