ARG81424

Human sFLT-1 / sVEGFR1 ELISA Kit

Human sFLT-1 / sVEGFR1 ELISA Kit for ELISA and Human

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Component

Cat No Component Name Package Temp
ARG81424-001 Antibody-coated microplate 8 X 12 strips 4°C. Unused strips should be sealed tightly in the air-tight pouch.
ARG81424-002 Standard 2 X 10 ng/vial 4°C
ARG81424-003 Standard/Sample diluent 30 ml (Ready to use) 4°C
ARG81424-004 Antibody conjugate concentrate (100X) 1 vial (100 µl) 4°C
ARG81424-005 Antibody diluent buffer 12 ml (Ready to use) 4°C
ARG81424-006 HRP-Streptavidin concentrate (100X) 1 vial (100 µl) 4°C
ARG81424-007 HRP-Streptavidin diluent buffer 12 ml (Ready to use) 4°C
ARG81424-008 25X Wash buffer 20 ml 4°C
ARG81424-009 TMB substrate 10 ml (Ready to use) 4°C (Protect from light)
ARG81424-010 STOP solution 10 ml (Ready to use) 4°C
ARG81424-011 Plate sealer 4 strips Room temperature

Overview

Product Description ARG81424 Human sFLT-1 / sVEGFR1 ELISA Kit is an Enzyme Immunoassay kit for the quantification of Human sFLT-1 / sVEGFR1 in serum, plasma (EDTA) and cell culture supernatants.
Tested Reactivity Hu
Tested Application ELISA
Specificity There is no detectable cross-reactivity with other relevant proteins.
Target Name sFLT1 / sVEGFR1
Conjugation HRP
Conjugation Note Substrate: TMB and read at 450 nm.
Sensitivity 78 pg/ml
Sample Type Serum, plasma (EDTA) and cell culture supernatants.
Standard Range 156 - 10000 pg/ml
Sample Volume 100 µl
Precision Intra-Assay CV: 5.5%
Inter-Assay CV: 6.4%
Alternate Names FLT-1; Vascular permeability factor receptor; Tyrosine-protein kinase receptor FLT; FLT; Vascular endothelial growth factor receptor 1; VEGFR1; VEGFR-1; Fms-like tyrosine kinase 1; EC 2.7.10.1; Tyrosine-protein kinase FRT

Application Instructions

Assay Time ~ 5 hours

Properties

Form 96 well
Storage Instruction Store the kit at 2-8°C. Keep microplate wells sealed in a dry bag with desiccants. Do not expose test reagents to heat, sun or strong light during storage and usage. Please refer to the product user manual for detail temperatures of the components.
Note For laboratory research only, not for drug, diagnostic or other use.

Bioinformation

Database Links

GeneID: 2321 Human FLT1

Swiss-port # P17948 Human Vascular endothelial growth factor receptor 1

Gene Symbol FLT1
Gene Full Name fms-related tyrosine kinase 1
Background This gene encodes a member of the vascular endothelial growth factor receptor (VEGFR) family. VEGFR family members are receptor tyrosine kinases (RTKs) which contain an extracellular ligand-binding region with seven immunoglobulin (Ig)-like domains, a transmembrane segment, and a tyrosine kinase (TK) domain within the cytoplasmic domain. This protein binds to VEGFR-A, VEGFR-B and placental growth factor and plays an important role in angiogenesis and vasculogenesis. Expression of this receptor is found in vascular endothelial cells, placental trophoblast cells and peripheral blood monocytes. Multiple transcript variants encoding different isoforms have been found for this gene. Isoforms include a full-length transmembrane receptor isoform and shortened, soluble isoforms. The soluble isoforms are associated with the onset of pre-eclampsia.[provided by RefSeq, May 2009]
Function 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. 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, proliferation of some types of cancer cells, but does not promote proliferation of normal fibroblasts (in vitro). 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. Likewise, isoforms lacking a transmembrane domain, such as isoform 2, isoform 3 and isoform 4, may function as decoy receptors for VEGFA. 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 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 and YES1, and may also phosphorylate CBL. Isoform 1 phosphorylates PLCG. Promotes phosphorylation of AKT1 at 'Ser-473'. Promotes phosphorylation of PTK2/FAK1. Isoform 7 has a truncated kinase domain; it increases phosphorylation of SRC at 'Tyr-418' by unknown means and promotes tumor cell invasion. [UniProt]
Highlight Related products:
VEGFR antibodies; VEGFR ELISA Kits;
New ELISA data calculation tool:
Simplify the ELISA analysis by GainData
PTM N-glycosylated.

Ubiquitinated after VEGFA-mediated autophosphorylation, leading to proteolytic degradation.

Autophosphorylated on tyrosine residues upon ligand binding. Autophosphorylation occurs in trans, i.e. one subunit of the dimeric receptor phosphorylates tyrosine residues on the other subunit. Phosphorylation at Tyr-1169 is important for interaction with PLCG. Phosphorylation at Tyr-1213 is important for interaction with PIK3R1, PTPN11, GRB2, and PLCG. Phosphorylation at Tyr-1333 is important for endocytosis and for interaction with CBL, NCK1 and CRK. Is probably dephosphorylated by PTPRB. [UniProt]

Specific References

Maternal Vascular Dysfunction in Congenital Heart Defects

ELISA / Human / Plasma

Yanli Liu et al.
Congenital Heart Disease,  (2023)

publication_link

 

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