Human VEGFR1-14/Flt1-14, soluble

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Size5 µg
Price150 €
SourceInsect cells
Purity Confirmation> 95% by SDS-PAGE & visualized by Coomassie stain
Length [aa]707
Molecular Weight105. kDa
N Terminal SequenceSKLKD
Biological ActivityThe activity of sFlt1-14 was determined by its ability to inhibit the VEGF-A-induced proliferation of HDLECs.
Species ReactivityHuman
ReconstitutionThe lyophilized sFlt1-14 is soluble in water and most aqueous buffers. The lyophilized sFlt1-14 should be reconstituted in water to a concentration not lower than 100µg/ml.
Stability and StorageLyophilized samples are stable for greater than six months at -20°C to -70°C. Reconstituted sFlt1-14 should be stored in working aliquots at -70°C. Avoid repeated freeze-thaw cycles!
Synonymssoluble vascular endothelial growth factor receptor-1; soluble FLT1; soluble VEGFR-1, sFlt1-14
DescriptionA human-specific splicing variant of vascular endothelial growth factor (VEGF) receptor 1 (Flt1) was discovered, producing a soluble receptor (designated sFlt1-14) that is qualitatively different from the previously described soluble receptor (sFlt1) and functioning as a potent VEGF inhibitor. sFlt1-14 is generated in a cell type-specific fashion, primarily in non-endothelial cells. Notably, in vascular smooth muscle cells, all Flt1 messenger RNA is converted to sFlt1-14, whereas endothelial cells of the same human vessel express sFlt1. sFlt1-14 expression by vascular smooth muscle cells is dynamically regulated as evidenced by its upregulation on coculture with endothelial cells or by direct exposure to VEGF. Increased production of soluble VEGF receptors during pregnancy is entirely attributable to induced expression of placental sFlt1-14 starting by the end of the first trimester. Expression is dramatically elevated in the placenta of women with preeclampsia, specifically induced in abnormal clusters of degenerative syncytiotrophoblasts known as syncytial knots, where it may undergo further messenger RNA editing. sFlt1-14 is the predominant VEGF-inhibiting protein produced by the preeclamptic placenta, accumulates in the circulation, and hence is capable of neutralizing VEGF in distant organs affected in preeclampsia. Together, these findings revealed a new natural VEGF inhibitor that has evolved in humans, possibly to protect non-endothelial cells from adverse VEGF signaling. Furthermore, the study uncovered the identity of a VEGF-blocking protein implicated in preeclampsia.
Uniprot IDP17948-3
Protein RefSeqNP_001153502.1
mRNA RefSeqNM_001160030.1


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