VEGFR2
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47233 | ENA |
REPOSITORIES: ENA
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Project description:The project concerns vascular endothelial growth factor (VEGF) signaling, which is dependent on binding of VEGF to VEGF receptor-2 (VEGFR2) and leads to activation of the receptor kinase and autophosphorylation. Previous mouse studies with the VEGFR-2 phosphorylation site mutation Y1212F showed reduced vascular stability. We here investigate with LC-MS proteomics which signal transduction pathway(s) are lost in the mutant by identifying proteins that bind to the Y1212F site.
2019-08-13 | PXD014517 | Pride
Project description:VEGFR2 Y949F (lung RNAseq - mice)
| PRJEB38638 | ENA
Project description:RNA sequencing of lung tissue from transgenic mice in order to investigate the effect of a single tyrosine to phenylalanine exchange in the endothelial receptor VEGFR2 at position Y949. This exchange creates a mouse with unleaky blood vessels which is an advantage in several diseases such as cancer and cardiovascular disease.
2020-06-12 | E-MTAB-9163 | biostudies-arrayexpress
Project description:The main goal of the project was to identify proteins binding to vascular endothelial growth factor receptor 2 (VEGFR2) phosphorylation site Y1173. Synthetic peptides, phosphorylated or not, covering different tyrosine phosphorylation sites in VEGFR2 were immobilized and incubated with cell lysates from human umbilical vein endothelial cells. Retained proteins were analyzed by mass spectrometry. Proteins specifically binding to pY1173 peptide were categorized with regard to the presence of an Src Homology 2 (SH2) domain and the main hits were validated in intact cells treated or not with VEGF, for their ability to bind to the activated wild type VEGFR2 but not to a mutant Y1173F VEGFR2. The role of the pY1173 binding partners in VEGF-regulated endothelial biology was further examined in vitro and in vivo.
2023-09-19 | PXD041024 | Pride
Project description:Transcriptome analysis was used to identify tumor-independent changes after treatment with mouse VEGFR2 neutralizing antibody.
2018-03-29 | GSE112467 | GEO
Project description:microRNA-126 is a microRNA predominately expressed by endothelial cells and controls angiogenesis. Unexpectedly, we found that mice deficient in miR-126 have a major impairment in their innate response to pathogen-associated nucleic acids, as well as HIV, which results in more widespread cell infection. Further examination revealed that this was due to miR-126 control of plasmacytoid DC (pDC) homeostasis and function, and that miR-126 regulates expression of TLR7, TLR9, NFkB1 and other innate response genes, as well as VEGF-receptor 2 (VEGFR2). Deletion of VEGFR2 on DCs resulted in reduced interferon production, supporting a role for VEGFR2 in miR-126 regulation of pDCs. These studies identify the miR-126/VEGFR2 axis as an important regulator of the innate response that operates through multiscale control of pDCs. Plasmactyoid dendritic cells were FACS-sorted from spleens from wildtype and miR-126 KO mice and their RNA extracted. RNA was amplified, labeled and hybridized to Mouse Gene 1.0 ST arrays with the data generation and quality control pipeline of 19 the Immunological Genome Project (www.immgen.org). Raw data were background-corrected and normalized using the RMA algorithm.
2013-11-24 | E-GEOD-51255 | biostudies-arrayexpress
Project description:microRNA-126 is a microRNA predominately expressed by endothelial cells and controls angiogenesis. Unexpectedly, we found that mice deficient in miR-126 have a major impairment in their innate response to pathogen-associated nucleic acids, as well as HIV, which results in more widespread cell infection. Further examination revealed that this was due to miR-126 control of plasmacytoid DC (pDC) homeostasis and function, and that miR-126 regulates expression of TLR7, TLR9, NFkB1 and other innate response genes, as well as VEGF-receptor 2 (VEGFR2). Deletion of VEGFR2 on DCs resulted in reduced interferon production, supporting a role for VEGFR2 in miR-126 regulation of pDCs. These studies identify the miR-126/VEGFR2 axis as an important regulator of the innate response that operates through multiscale control of pDCs.
2013-11-24 | GSE51255 | GEO
Project description:Single cell RNA sequencing for dental pulp cells of first molars in control and endothelial Vegfr2 knockout mice at P12
2022-02-03 | GSE181175 | GEO
Project description:Angiogenesis, the formation of new blood vessels from pre-existing ones, is a complex and demanding biological process that plays an important role in physiological as well as pathological settings such as cancer and ischemia. Given its critical role, the regulation of endothelial growth factor receptor (e.g. VEGFR2, FGFR1) represents important mechanisms for the control of angiogenesis. Recent evidences support cell metabolism as a critical regulator of angiogenesis. However, it is unknown how glutamine metabolism regulates growth factor receptor expression. Here, by using genetic and pharmacological approaches, we show that glutaminolysis and glutamate-dependent transaminases (TAs) support alpha-ketoglutarate (αKG) levels and are critical regulators of angiogenic response during pathological conditions. Indeed, the endothelial specific blockage of GLS1 impairs ischemic and tumor angiogenesis by suppressing VEGFR2 translation via mTORC1-dependent pathway. Lastly, we discover that ECs catabolized the glutamine-derived glutamate via phosphoserine aminotransferase 1 (PSAT1) as crucial to support VEGFR2 translation. These findings identify glutamine anaplerosis and TA activity as a critical regulator of growth factor receptor translation in normal and pathological angiogenesis. We anticipate our studies to be a starting point for novel anti-angiogenesis approaches based on GLS1/PSAT1 inhibitor treatments to overcome anti-VEGF therapies resistance.
2022-04-22 | PXD022379 | Pride