Mouse Vascular endothelial cell growth factor receptor 1,VEGFR-1/Flt1 ELISA kit

Code CSB-E04762m
Size 96T,5×96T,10×96T
Trial Size 24T ELISA kits trial application
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Product Details


This Mouse VEGFR-1/Flt1 ELISA Kit was designed for the quantitative measurement of Mouse VEGFR-1/Flt1 protein in serum, plasma, tissue homogenates. It is a Sandwich ELISA kit, its detection range is 1.56 ng/mL-100 ng/mL and the sensitivity is 0.39 ng/mL.

Target Name fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
Alternative Names Flt1 ELISA Kit; Emrk2 ELISA Kit; Flt ELISA Kit; Vegfr1 ELISA Kit; Vascular endothelial growth factor receptor 1 ELISA Kit; VEGFR-1 ELISA Kit; EC ELISA Kit; Embryonic receptor kinase 2 ELISA Kit; Fms-like tyrosine kinase 1 ELISA Kit; FLT-1 ELISA Kit; Tyrosine-protein kinase receptor FLT ELISA Kit
Abbreviation VEGFR-1/Flt1
Uniprot No. P35969
Species Mus musculus (Mouse)
Sample Types serum, plasma, tissue homogenates
Detection Range 1.56 ng/mL-100 ng/mL
Sensitivity 0.39 ng/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Cardiovascular
Assay Principle quantitative
Measurement Sandwich
Intra-assay Precision (Precision within an assay): CV%<8%        
Three samples of known concentration were tested twenty times on one plate to assess.    
Inter-assay Precision (Precision between assays): CV%<10%        
Three samples of known concentration were tested in twenty assays to assess.      
To assess the linearity of the assay, samples were spiked with high concentrations of mouse VEGFR-1/Flt1 in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.  
  Sample Serum(n=4)    
1:1 Average % 90    
Range % 85-95    
1:2 Average % 103    
Range % 100-106    
1:4 Average % 85    
Range % 80-90    
1:8 Average % 104    
Range % 100-107    
The recovery of mouse VEGFR-1/Flt1 spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.  
Sample Type Average % Recovery Range    
Serum (n=5) 84 80-90    
EDTA plasma (n=4) 108 104-112    
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.  
ng/ml OD1 OD2 Average Corrected    
100 2.602 2.631 2.617 2.495    
50 2.003 2.068 2.036 1.914    
25 1.339 1.361 1.350 1.228    
12.5 0.785 0.779 0.782 0.660    
6.25 0.452 0.461 0.457 0.335    
3.12 0.284 0.291 0.288 0.166    
1.56 0.186 0.187 0.187 0.065    
0 0.120 0.123 0.122      
ELISA Data Analysis Watch ELISA data processing video & download Curve Expert if needed
and FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 3-5 working days

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Target Background

(From Uniprot)
Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFB and PGF, and plays an essential role in the development of embryonic vasculature, the regulation of angiogenesis, cell survival, cell migration, macrophage function, chemotaxis, and cancer cell invasion. Acts as a positive regulator of postnatal retinal hyaloid vessel regression. May play an essential role as a negative regulator of embryonic angiogenesis by inhibiting excessive proliferation of endothelial cells. Can promote endothelial cell proliferation, survival and angiogenesis in adulthood. Its function in promoting cell proliferation seems to be cell-type specific. Promotes PGF-mediated proliferation of endothelial cells, and proliferation of some types of cancer cells, but does not promote proliferation of normal fibroblasts. Has very high affinity for VEGFA and relatively low protein kinase activity; may function as a negative regulator of VEGFA signaling by limiting the amount of free VEGFA and preventing its binding to KDR. Modulates KDR signaling by forming heterodimers with KDR. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, leading to the activation of phosphatidylinositol kinase and the downstream signaling pathway. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Phosphorylates SRC, YES1 and PLCG, and may also phosphorylate CBL. Promotes phosphorylation of AKT1 and PTK2/FAK1.
Gene References into Functions
  1. excessive sFlt1 and lack of eNOS synergistically induce hepatic dysfunction and thrombocytopenia, suggesting a novel role for VEGF and nitric oxide signaling in hepatocyte-endothelial cross-talk in health and in liver injury states. PMID: 29311569
  2. Motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF via their own expression of sFlt1. PMID: 28262664
  3. inducible endothelial genetic deletion of Neuropilin1 (Nrp1) and Vascular endothelial growth factor receptor 1 (Vegfr1; also known as Flt1) renders mice resistant to diet-induced obesity. PMID: 30093598
  4. Results show that Flt1 heterozygosity causes embryonic edema with enhanced vascular permeability. It can also be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype. PMID: 27251772
  5. Our study suggests that "migration" of the placenta is derived from placental degeneration at the caudal part of the placenta, and sFlt-1 plays a role in this placental degeneration. PMID: 29409879
  6. This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 in the coronary vascular system during development and after MI; thus, this study suggests that these factors have distinct and important functions in coronary angiogenesis. PMID: 29158084
  7. sFlt-1 overexpression in Padi4(-/-) mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation. PMID: 28007693
  8. endothelial dysfunction due to high circulating sFLT1 may be the primary event leading to enhanced vasoconstrictor sensitivity that is characteristic of preeclampsia PMID: 27270170
  9. Flt1 has a role in blood vessel anastomosis during angiogenesis PMID: 28246215
  10. Esomeprazole decreased blood pressure in a transgenic mouse model where human sFlt-1 was overexpressed in placenta. PPIs upregulated endogenous antioxidant defenses and decreased cytokine secretion from placental tissue and endothelial cells. PMID: 28115513
  11. First-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully validated in an orthotopic murine tumor model. PMID: 27390161
  12. these results suggest that VEGFR1 signaling plays a role in regulating the balance between macrophage phenotypes in streptozotocin -induced diabetic wounds, prevents impaired diabetic wound healing, and promotes angiogenesis/lymphangiogenesis. PMID: 27085138
  13. These data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B to VEGFR1. PMID: 26928042
  14. Flt1/VEGF-A signalling has stage-specific effects on vascular morphogenesis. PMID: 27142980
  15. IL-35 treatment reduced collagen-induced arthritis via inhibiting vascular endothelial growth factor and its receptors PMID: 26922678
  16. the VEGFR-1 tyrosine kinase signaling has an effect on angiogenesis. PMID: 26898435
  17. data suggest that sFlt-1 may have a therapeutic effect on AS, resulting from suppression of VEGF signaling-mediated recruitment of circulating monocytes/macrophages PMID: 26600037
  18. that Flt-1 plays a critical role in cardiac hypertrophy induced by pressure overload via the activation of AKT PMID: 26017635
  19. Flt-1 appears to play a role in oxidative stress, which promotes apoptosis of trophoblasts PMID: 26203176
  20. This article reviews the current evidence on the clinical utility of the sFlt-1/PlGF ratio at different points in pregnancy and, accordingly, make a proposal for its clinical implementation. [review] PMID: 26287164
  21. Circulating sFlt-1 is generated as a result of myocardial injury and subsequent heart failure development. PMID: 26699385
  22. A reduction in sFLT-1 triggers blood vessels to grow into the photoreceptor layer from above or below. PMID: 23795287
  23. The hypoxia-induced rise in sFlt-1 levels seems not to be mediated by IL-6 in vivo. PMID: 25415335
  24. FLT1 inhibition reduces tumor metastatic efficiency even after initial seeding, suggesting that these pathways represent therapeutic targets in metastatic disease. PMID: 26261265
  25. Vandetanib treatment can reduce arteriosclerosis induced by abdominal aorta transplantation by blocking VEGFR1 and VEGFR2 in endothelial progenitor cells PMID: 25437886
  26. Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity through selective activation of VEGF receptor 1 (VEGFR1) expressed in sensory neurons in human cancer and mouse models. PMID: 26058077
  27. We examined the differential expression of soluble fms-like tyrosine kinase 1 (Flt-1) using 35 pups from six normal pregnant mice. Expression of sFlt-1 was significantly different between litters PMID: 24702464
  28. Studied the role of VEGF signaling in compensatory lung growth. PMID: 25642830
  29. VEGFR1 activation is a potential therapeutic strategy for promoting liver repair and sinusoidal restoration after acute liver injury. PMID: 25162491
  30. Endothelial production of sFlt-1 is reduced in chronic kidney disease promoting atherosclerotic processes. PMID: 24048373
  31. These data were supported further by murine chromatin immunoprecipitation demonstrating that FLT1 is a target of Nr2e3, a nuclear receptor gene implicated in regulating an AMD pathway. PMID: 24812550
  32. Up-regulated Glrx inhibits VEGF signaling by increased Flt1 causing impaired vascularization. PMID: 24482236
  33. VEGFR1 signaling becomes functional starting at the early stages of laser-induced choroidal neovascularization, but VEGFR2 is not present until the relatively late stages. PMID: 23977149
  34. The results establish that Vegfr1 produced in the endocardium negatively regulates embryonic coronary angiogenesis, possibly by limiting the Vegf-Notch signaling. PMID: 23894673
  35. Data indicate that VEGF-B is a high-affinity VEGFR-1 ligand that, unlike PlGF, cannot efficiently induce signaling downstream of VEGFR-1. PMID: 23821770
  36. Prenatal hypoxia insults, at least in late gestation, influence pulmonary VEGF and VEGF receptor expression through the down-regulation of HIF pathways and impair fetal lung growth and maturation. PMID: 23548588
  37. Elevated Notch signaling downstream of perturbed VEGF signaling contributes to aberrant flt-1(-/-) blood vessel formation. PMID: 23744993
  38. Macrophage Wnt-Calcineurin-Flt1 signaling regulates mouse wound angiogenesis and repair. PMID: 23303818
  39. The significant upregulation of VEGFR1 surface levels after skeletal muscle ischemia indicates that VEGFR1 indeed plays a critical role in the ischemia-induced perfusion recovery process, a process that includes both angiogenesis and arteriogenesis. PMID: 23376830
  40. Data indicate that the combination of Flt1(+)/Flt4(+) best identified and facilitated enrichment for Isl1(+)/Nkx2.5(+) cardiovascular progenitor cells (CPCs) from embryonic hearts and differentiating induced pluripotent stem cell (iPSC). PMID: 23056209
  41. analysis of the balance of anti-angiogenic or modulatory (VEGFR1) and pro-angiogenic (VEGFR2) signaling in skeletal muscle and endothelial cells PMID: 22984559
  42. VEGFR-1 blockade and genetic deletion of the tyrosine kinase domain of VEGFR-1 resulted in enhanced tumor angiogenesis. PMID: 23267058
  43. The decrease in PlGF and VEGF coupled with the increase in sFlt-1 suggests that Ang-(1-7) may serve as a novel anti-angiogenic therapy for prostate cancer. PMID: 22644934
  44. show that perivascular cells and pericytes that support endothelial cells in various tissues produce sFLT1. Deletion of Flt1 from one population of specialized pericytes, the glomerular podocytes, in mice causes profound reorganization of the podocyte actin cytoskeleton and proteinuria, reflecting pericyte dysfunction. PMID: 23063127
  45. Chemical stabilization of HIF-2alpha using an inhibitor of prolyl hydroxylase domain 3 (an upstream inhibitor of HIF-2alpha activation) increases VEGFR-1 production from granulocyte macrophage-colony stimulating factor(GM-CSF)-stimulated macrophages. PMID: 22869907
  46. Stria vascularis vasculature and expression of VEGF, Flt-1, and Flk-1 do not change with age, and there appears to be no apical to basal differential expression. PMID: 22569048
  47. In a postinfarct ischemic cardiomyopathy model, VEGFR-1 deficiency supports robust angiogenesis and protects against myocardial infarction. PMID: 22753193
  48. VEGFR1_MOe13 elevated sFlt-1 mRNA expression and suppressed mbFlt-1 mRNA expression in vitro in multiple cellular backgrounds (p<0.001). PMID: 22438952
  49. identified downregulation of vascular endothelial growth factor receptor 1 (VEGFR1), which acts as a decoy receptor for VEGF, as a key mediator of the endothelial response to lipoproteins PMID: 22581286
  50. IL-17A signaling played a major part in causing corneal neovascularization by shifting the balance between VEGF-A and its soluble receptor. PMID: 22379030

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Subcellular Location Cell membrane; Single-pass type I membrane protein. Endosome.
Protein Families Protein kinase superfamily, Tyr protein kinase family, CSF-1/PDGF receptor subfamily
Database Links

KEGG: mmu:14254

STRING: 10090.ENSMUSP00000031653

UniGene: Mm.389712

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