FLT1 Antibody, FITC conjugated

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Cat. No.
BT1971009
Synonyms
EC 2.7.10.1 antibody; FLT 1 antibody; FLT antibody; Flt-1 antibody; FLT1 antibody; Fms like tyrosine kinase 1 antibody; Fms related tyrosine kinase 1 antibody; Fms related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor) antibody; Fms related tyrosine kinase 1 vascular endothelial growth factor/vascular permeability factor receptor antibody; Fms-like tyrosine kinase 1 antibody; FRT antibody; Soluble VEGF receptor 1 14 antibody; Soluble VEGFR1 variant 2 antibody; Soluble VEGFR1 variant 21 antibody; Tyrosine protein kinase FRT antibody; Tyrosine protein kinase receptor FLT antibody; Tyrosine-protein kinase FRT antibody; Tyrosine-protein kinase receptor FLT antibody; Vascular endothelial growth factor receptor 1 antibody; Vascular endothelial growth factor vascular permeability factor receptor antibody; Vascular permeability factor receptor 1 antibody; Vascular permeability factor receptor antibody; VEGFR 1 antibody; VEGFR-1 antibody; VEGFR1 antibody; VGFR1_HUMAN antibody
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Product Specs

Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
Typically, we can ship the products within 1-3 business days after receiving your order. Delivery time may vary depending on the shipping method and destination. Please consult your local distributors for specific delivery details.
Synonyms
EC 2.7.10.1 antibody; FLT 1 antibody; FLT antibody; Flt-1 antibody; FLT1 antibody; Fms like tyrosine kinase 1 antibody; Fms related tyrosine kinase 1 antibody; Fms related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor) antibody; Fms related tyrosine kinase 1 vascular endothelial growth factor/vascular permeability factor receptor antibody; Fms-like tyrosine kinase 1 antibody; FRT antibody; Soluble VEGF receptor 1 14 antibody; Soluble VEGFR1 variant 2 antibody; Soluble VEGFR1 variant 21 antibody; Tyrosine protein kinase FRT antibody; Tyrosine protein kinase receptor FLT antibody; Tyrosine-protein kinase FRT antibody; Tyrosine-protein kinase receptor FLT antibody; Vascular endothelial growth factor receptor 1 antibody; Vascular endothelial growth factor vascular permeability factor receptor antibody; Vascular permeability factor receptor 1 antibody; Vascular permeability factor receptor antibody; VEGFR 1 antibody; VEGFR-1 antibody; VEGFR1 antibody; VGFR1_HUMAN antibody
Target Names
FLT1
Uniprot No.
P17948

Target Background

Function
Fms-like tyrosine kinase 1 (FLT1), also known as vascular endothelial growth factor receptor 1 (VEGFR1), is a tyrosine-protein kinase that acts as a cell-surface receptor for VEGF-A, VEGF-B, and PGF. FLT1 plays a crucial role in embryonic vasculature development, angiogenesis regulation, cell survival, cell migration, macrophage function, chemotaxis, and cancer cell invasion. It acts as a positive regulator of postnatal retinal hyaloid vessel regression. Additionally, FLT1 may play an essential role as a negative regulator of embryonic angiogenesis by inhibiting excessive proliferation of endothelial cells. In adulthood, it promotes endothelial cell proliferation, survival, and angiogenesis. Its function in promoting cell proliferation appears to be cell-type specific. It promotes PGF-mediated proliferation of endothelial cells and proliferation of certain types of cancer cells, but does not promote the proliferation of normal fibroblasts (in vitro). FLT1 exhibits a very high affinity for VEGF-A and relatively low protein kinase activity. It may function as a negative regulator of VEGF-A signaling by limiting the amount of free VEGF-A and preventing its binding to KDR. FLT1 modulates KDR signaling by forming heterodimers with KDR. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG results in the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate, and the activation of protein kinase C. FLT1 mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, leading to activation of phosphatidylinositol kinase and the downstream signaling pathway. It also mediates activation of MAPK1/ERK2, MAPK3/ERK1, and the MAP kinase signaling pathway, as well as the AKT1 signaling pathway. FLT1 phosphorylates SRC and YES1, and may also phosphorylate CBL. It promotes phosphorylation of AKT1 at 'Ser-473'. FLT1 promotes phosphorylation of PTK2/FAK1. It also phosphorylates PLCG. FLT1 may function as a decoy receptor for VEGF-A. It has a truncated kinase domain; it increases phosphorylation of SRC at 'Tyr-418' by unknown means and promotes tumor cell invasion.
Gene References Into Functions
  1. These results indicate that sFlt-1 up-regulation by VEGF may be mediated by the VEGF/Flt-1 and/or VEGF/KDR signaling pathways. PMID: 29497919
  2. Serum sFlt-1 can be used as a prognostic marker to predict the occurrence of complications of preeclampsia. PMID: 30032672
  3. The ratio of sFlt-1/sEGFR could be used as a novel candidate biochemical marker in monitoring the severity of preterm preeclampsia. sEndoglin and sEGFR may be involved in the pathogenesis of small for gestational age in preterm preelampsia. PMID: 30177039
  4. A contingent strategy of measuring the sFlt-1/PlGF ratio at 24-28weeks in women previously selected by clinical factors and uterine artery Doppler enables an accurate prediction of preeclampsia/fetal growth restriction. PMID: 30177066
  5. Dynamic regulation of mVEGFR1 stability and turnover in blood vessels impacts angiogenesis. PMID: 28589930
  6. Study shows that soluble VEGF receptor 1 (sVEGFR-1/ soluble fms-like tyrosine kinase 1 [sFlt-1]) showed a cytotoxic effect on BeWo cells. Results suggest that sFLT-1 could be therapeutic for malignant tumors. PMID: 28322131
  7. A single measurement of sFlt-1/PlGF ratio at third trimester to predict pre-eclampsia and intrauterine growth retardation occurring after 34weeks of pregnancy. PMID: 29674192
  8. sFlt1 was produced in significant amounts by preeclamptic peripheral blood mononuclear leukocytes, and ex vivo studies show that the placenta induces this over-expression. In contrast, exposure to PBMCs appears to decrease sFlt1 production by preeclamptic placenta. PMID: 29674197
  9. The levels of sFlt-1, PlGF, and the sFlt-1/PlGF ratio in pre-eclamptic women with an onset at < 32 weeks were significantly different from those in women with an onset at >/=32-33 weeks. PMID: 29674208
  10. These results showed that arginase controlled sFlt-1 elevation to some extent. PMID: 29548823
  11. These results suggest that VM formation is increased by EBVLMP1 via VEGF/VEGFR1 signaling and provide additional information to clarify the role of EBVLMP1 in nasopharyngeal carcinoma (NPC)pathophysiology. PMID: 29749553
  12. An sFlt-1:PlGF ratio above 655 is not predictive of impaired perinatal outcomes, and insufficiently reliable for predicting outcomes in cases with clinical signs of preeclampsia. PMID: 29523274
  13. The maternal sFlt-1 to PlGF ratio in women with hypertensive disorders in pregnancy carries prognostic value for the development of preeclampsia. PMID: 29523275
  14. VEGFA activates VEGFR1 homodimers and AKT, leading to a cytoprotective response, whilst abluminal VEGFA induces vascular leakage via VEGFR2 homodimers and p38. PMID: 29734754
  15. Metformin's dual effect in hyperglycemia-chemical hypoxia is mediated by direct effect on VEGFR1/R2 leading to activation of cell migration through MMP16 and ROCK1 upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4, components of VEGF signaling cascades. PMID: 29351188
  16. Additionally, LVsFlt1MSCs inhibited tumor growth and prolonged survival in an hepatocellular carcinoma (HCC) mouse model via systemic injection. Overall, the present study was designed to investigate the potential of LVsFlt1MSCs for antiangiogenesis gene therapy in HCC. PMID: 28849176
  17. Review of the role of dysregulation at the Fms-like tyrosine kinase 1 locus in the fetal genome (likely in the placenta) in conferring genetic predisposition to preeclampsia. PMID: 29138037
  18. VEGF and VEGFR1 levels in different regions of the normal and preeclampsia placentae. PMID: 28770473
  19. High PlGF and/or low sFlt-1/PlGF may be used to diagnose Peripartum Cardiomyopathy. PMID: 28552862
  20. Results demonstrate that short-activating RNA targeting the flt-1 promoter increased sFlt-1 mRNA and protein levels, while reducing VEGF expression. This was associated with suppression of human umbilical vascular endothelial cell (HUVEC) proliferation and cell cycle arrest at the G0/G1 phase. HUVEC migration and tube formation were also suppressed by Flt a-1. PMID: 29509796
  21. In this context, our results demonstrate that D16F7 markedly inhibits chemotaxis and invasiveness of GBM cells and patient-derived GBM stem cells (GSCs) in response to VEGF-A and PlGF, suggesting that VEGFR-1 might represent a suitable target that deserves further investigation for GBM treatment. PMID: 28797294
  22. Study showed that term deliveries, higher soluble fms-like tyrosine kinase 1 (sFlt1) concentrations were associated with a smaller uterine artery resistance indices (RI) at the subsequent visit. For preterm delivery, higher sFlt1 concentrations were associated with a larger uterine artery RI. PMID: 28335685
  23. Elevated in preeclampsia and fetal growth restriction. PMID: 27865093
  24. Studied serum levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) as markers for early diagnosis of preeclampsia. PMID: 29267975
  25. This prospective observational study compare urine nephrin:creatinine ratio (NCR, ng/mg) with serum soluble fms-like tyrosine kinase-1:placental growth factor ratio (FPR, pg/pg) for preeclampsia (PE) prediction among unselected asymptomatic pregnant women in 2(nd) trimester. PMID: 27874074
  26. A high sFlt-1/PlGF ratio was associated with adverse outcomes and a shorter duration to delivery in early-onset fetal growth restriction. PMID: 28737473
  27. Serum from type 2 diabetics reduced Akt/VEGFR-1 protein expression in endothelial progenitor cells. PMID: 28732797
  28. The VEGF/sVEGF-R1 ratio in follicular fluid on the day of oocyte retrieval in women undergoing IVF procedure, regardless of the type of stimulation protocol, might predict the risk of developing ovarian hyperstimulation syndrome (OHSS). To the best of our knowledge this is the first paper in the literature to show interplay among VEGF, EG-VEGF and sVEGF-R1 and the correlation between their concentration and OHSS risk. PMID: 28820403
  29. Plasma level not associated with placenta size. PMID: 28613009
  30. The difference between the pro- (VEGF165a) and antiangiogenic (VEGF165b) VEGF isoforms and its soluble receptors for severity of diabetic retinopathy, is reported. PMID: 28680264
  31. Detectable amounts are produced by endometrial stromal cells (ESC)); expression is turned off during decidualization; ESC decidualization and resulting sFlt1 expression are a reversible phenomenon. PMID: 28494174
  32. High sFlt-1 concentrations may account for diminished maternal serum PlGF levels. PMID: 28494189
  33. Upregulated tenfold in preeclamptic tissue. PMID: 28067578
  34. Upregulation of sVEGFR-1 with concomitant decline of PECAM-1 and sVEGFR-2 levels in preeclampsia compared to normotensive pregnancies, irrespective of the HIV status. PMID: 28609170
  35. In patients with hypertensive disorders of pregnancy, those in the highest tertile of mean arterial pressure had the highest serum levels of sFlt1 and sEng. PMID: 28609171
  36. Likely that in early onset pre-eclampsia, increased maternal sFlt-1 concentrations are the primary reason for diminished maternal serum-free PlGF levels. PMID: 28609172
  37. Based on these data, we conclude that the rs9943922 SNP in the FLT1 gene does not result in a large difference in FLT1 protein levels, regardless of whether it is the soluble or the membrane bound form. PMID: 28949775
  38. Report sensitivity of sFlt-1/PlGF ratio for diagnosis of preeclampsia and fetal growth restriction. PMID: 28501276
  39. 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
  40. The association of VEGFR1 rs9582036 and rs9554320 with the outcome of sunitinib in mRCC patients did not reach the threshold for statistical significance, and therefore, both genetic variants have limited use as biomarkers for prediction of sunitinib efficacy. PMID: 27901483
  41. Placental sFLT-1 expression is upregulated in approximately 28% of non-preeclamptic pregnancies complicated by small for gestational age infants. These pregnancies showed increased placental vascular pathology, more umbilical Doppler abnormalities, and earlier delivery with lower birthweight. PMID: 28454690
  42. This study demonstrated that the baseline of sFlt-1 was significantly correlated with soft neurologic signs and right entorhinal volume but not other baseline clinical/brain structural measures in patient with psychosis. PMID: 27863935
  43. By comparing in vivo data with immunohistochemical analysis of excised tumors we found an inverse correlation between 99mTc-VEGF165 uptake and VEGF histologically detected, but a positive correlation with VEGF receptor expression (VEGFR1). PMID: 28498441
  44. sFLT-1 represents a link between angiogenesis, endothelial dysfunction, and subclinical atherosclerosis. Measurement of sFLT-1 as a marker of vascular dysfunction in beta-TI may provide utility for early identification of patients at increased risk of cardiopulmonary complications. PMID: 28301910
  45. Icrucumab and ramucirumab are recombinant human IgG1 monoclonal antibodies that bind vascular endothelial growth factor (VEGF) receptors 1 and 2 (VEGFR-1 and -2), respectively. VEGFR-1 activation on endothelial and tumor cell surfaces increases tumor vascularization and growth and supports tumor growth via multiple mechanisms, including contributions to angiogenesis and direct promotion of cancer cell proliferation. PMID: 28220020
  46. sFLT-1 e15a splice variant is seen only in humans and is principally expressed in the placenta, making it likely to be the variant chiefly responsible for the clinical features of early-onset pre-eclampsia. (Review) PMID: 27986932
  47. Significant reduction in sVEGFR-1 levels after renal denervation procedure for hypertension. PMID: 27604660
  48. Cases with high MDSC infiltration, which was inversely correlated with intratumoral CD8(+) T-cell infiltration, exhibited shorter overall survival. In a mouse model, intratumoral MDSCs expressed both VEGFR1 and VEGFR2. VEGF expression in ovarian cancer induced MDSCs, inhibited local immunity, and contributed to poor prognosis. PMID: 27401249
  49. Circulating tissue transglutaminase is associated with sFlt-1, soluble endoglin and VEGF in the maternal circulation of preeclampsia patients, suggesting that tTG may have a role in the pathogenesis of PE. PMID: 27169826
  50. The authors observed direct damage caused by sFLT1 in tumour cells. They exposed several kinds of cells derived from ovarian and colorectal cancers as well as HEK293T cells to sFLT1 in two ways, transfection and exogenous application. The cell morphology and an lactate dehydrogenase assay revealed cytotoxicity. PMID: 27103202

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Database Links

HGNC: 3763

OMIM: 165070

KEGG: hsa:2321

STRING: 9606.ENSP00000282397

UniGene: Hs.594454

Involvement In Disease
Can contribute to cancer cell survival, proliferation, migration, and invasion, and tumor angiogenesis and metastasis. May contribute to cancer pathogenesis by promoting inflammatory responses and recruitment of tumor-infiltrating macrophages.; DISEASE: Note=Abnormally high expression of soluble isoforms (isoform 2, isoform 3 or isoform 4) may be a cause of preeclampsia.
Protein Families
Protein kinase superfamily, Tyr protein kinase family, CSF-1/PDGF receptor subfamily
Subcellular Location
[Isoform 1]: Cell membrane; Single-pass type I membrane protein. Endosome. Note=Autophosphorylation promotes ubiquitination and endocytosis.; [Isoform 2]: Secreted.; [Isoform 3]: Secreted.; [Isoform 4]: Secreted.; [Isoform 5]: Cytoplasm.; [Isoform 6]: Cytoplasm.; [Isoform 7]: Cytoplasm.
Tissue Specificity
Detected in normal lung, but also in placenta, liver, kidney, heart and brain tissues. Specifically expressed in most of the vascular endothelial cells, and also expressed in peripheral blood monocytes. Isoform 2 is strongly expressed in placenta. Isoform

Q&A

What validation parameters are essential when implementing FLT1-FITC antibodies in flow cytometry?

Three-tier validation should include:

  • Specificity confirmation: Compare staining patterns in FLT1-positive (e.g., HUVECs) versus negative control cells .

  • Titration optimization: Test concentrations from 1-5 µl/10^6 cells using serial dilutions .

  • Competition assays: Pre-incubate with recombinant FLT1 extracellular domain (10 µg/mL for 1 hr) to confirm signal reduction .

Validation StepCritical ParametersTypical Results
SpecificityΔMFI (Positive - Negative)≥10-fold difference
TitrationSignal-to-noise ratio≥5:1 at working concentration
Competition% Signal inhibition≥70% reduction

Reference the antibody's cross-reactivity profile with homologous receptors (VEGFR2/KDR) using Western blotting .

How should researchers control for autofluorescence when using FLT1-FITC in primary endothelial cells?

Implement a four-step compensation strategy:

  • Unstained controls: Establish baseline autofluorescence across FITC (488/515 nm) and adjacent channels .

  • Single-stained compensation beads: Create spectral overlap profiles using anti-species capture beads .

  • Chemical quenching: Treat cells with 0.1% trypan blue (5 min) to reduce non-specific signal .

  • Time-resolved acquisition: Use delay times >5 ns to separate FITC fluorescence from cellular lipofuscin .

What experimental approaches resolve contradictory data in FLT1-mediated signaling studies?

Contradictions often arise from:

  • Ligand specificity conflicts:

    • Validate binding kinetics using surface plasmon resonance (SPR) with 100 nM VEGF-A vs PlGF-2 .

    • Employ receptor dimerization assays (FRET efficiency ≥15% indicates heterodimerization with VEGFR2) .

  • Phosphorylation discrepancies:

    • Combine immunoprecipitation (IP) with Phos-tag® SDS-PAGE (5% gel) to separate pY1213 vs pY1333 isoforms .

    • Use temporal profiling (0-60 min post-stimulation) at 2-min intervals .

  • Pathological context variability:

    • Compare angiogenic responses in 3D microfluidic models (20 dyn/cm² shear stress) versus static cultures .

How can researchers optimize FLT1-FITC for multiplexed CyTOF applications while maintaining epitope integrity?

Follow this metal-tagging protocol:

  • Conjugate stability: Chelate FITC with X8 polymers (2 hr, 4°C) before attaching ^89Y isotopes .

  • Signal amplification: Apply lanthanide-loaded nanoparticles (3:1 Ab:particle ratio) for low-abundance targets .

  • Validation controls:

    • Compare signal linearity across 4-log cell number range (10^2-10^5 cells)

    • Test antigen retrieval compatibility (pH 9.0 Tris-EDTA vs enzymatic methods)

ParameterCyTOF-Optimized ProtocolStandard Flow Protocol
Incubation time45 min (RT)30 min (4°C)
Permeabilization0.25% saponin (10 min)0.1% Triton X-100 (5 min)
Signal threshold≥200 counts/channel≥10^3 MFI

What methodologies confirm FLT1-FITC specificity in complex tissue matrices?

Implement orthogonal validation:

  • Proximity ligation assay (PLA):

    • Use Duolink® reagents with anti-FITC PLUS and MINUS probes (30 nm detection radius) .

    • Validate >5 puncta/cell in VEGF-stimulated vs unstimulated endothelia .

  • Multispectral imaging:

    • Apply Nuance® FX system with 20 nm bandwidth filters (470-650 nm range) .

    • Calculate spectral unmixing residuals <5% for FITC/autofluorescence separation .

  • Functional blockade:

    • Pre-treat tissues with 10 µg/mL soluble FLT1 extracellular domain (sFlt-1) for 2 hr .

    • Require ≥80% signal reduction in competitive inhibition assays .

How to address non-linear FLT1-FITC staining gradients in vascular zonation studies?

Three corrective measures:

  • Perfusion-controlled staining:

    • Deliver antibody via peristaltic pump (0.5 mL/min) for 30 min .

    • Maintain physiological pressure (80-120 mmHg) using ex vivo organ culture systems .

  • Quenching protocol optimization:

    • Use 0.3 M glycine (pH 2.5) for 5 min followed by 100 mM NH4Cl neutralization .

  • Computational correction:

What novel findings suggest FLT1-FITC utility in viral pathogenesis studies?

Recent discoveries demonstrate:

  • SARS-CoV-2 spike protein interaction:

    • SPR shows Kd = 12.5 nM between RBD and sFLT1 .

    • Co-immunoprecipitation efficiency reaches 38% in ACE2/Flt-1 co-expressing cells .

  • Signaling cascade activation:

    • Phospho-tyrosine profiling reveals pY1213 hyperphosphorylation (3.8-fold increase) post-spike exposure .

  • Therapeutic implications:

    • FLT1-FITC enables tracking of spike-induced endothelial dysfunction in microphysiological systems .

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