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

  • 中文名称:
    小鼠血管内皮细胞生长因子受体1(VEGFR-1/Flt1)酶联免疫试剂盒
  • 货号:
    CSB-E04762m
  • 规格:
    96T/48T
  • 价格:
    ¥3200/¥2500
  • 其他:

产品详情

  • 产品描述:

    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.

  • 别名:
    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 2.7.10.1 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
  • 缩写:
  • Uniprot No.:
  • 种属:
    Mus musculus (Mouse)
  • 样本类型:
    serum, plasma, tissue homogenates
  • 检测范围:
    1.56 ng/mL-100 ng/mL
  • 灵敏度:
    0.39 ng/mL
  • 反应时间:
    1-5h
  • 样本体积:
    50-100ul
  • 检测波长:
    450 nm
  • 研究领域:
    Cardiovascular
  • 测定原理:
    quantitative
  • 测定方法:
    Sandwich
  • 精密度:
    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.      
                   
  • 线性度:
    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    
  • 回收率:
    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    
                   
                   
  • 标准曲线:
    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      
  • 数据处理:
  • 货期:
    3-5 working days

产品评价

靶点详情

  • 功能:
    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.
  • 基因功能参考文献:
    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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  • 亚细胞定位:
    Cell membrane; Single-pass type I membrane protein. Endosome.
  • 蛋白家族:
    Protein kinase superfamily, Tyr protein kinase family, CSF-1/PDGF receptor subfamily
  • 数据库链接: