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Recombinant Human VEGFR3/FLT4 protein (hFc Tag)(HPLC verified)

Species

Human

Purity

>95 %, SDS-PAGE
>90 %, SEC-HPLC

Tag

hFc Tag

Activity

EC50: 2-9 ng/mL

Cat no : Eg0353



Product Information

Purity >95 %, SDS-PAGE
>90 %, SEC-HPLC
Endotoxin <0.1 EU/μg protein, LAL method
Activity
Immobilized Human VEGFC (Myc tag, His tag) at 2 μg/mL (100 μL/well) can bind Human VEGFR3 (hFc tag) with a linear range of 2-9 ng/mL.
Expression HEK293-derived Human VEGFR3 protein Tyr25-Ile776 & Ser473-Ile776 (Accession# P35916-1) with a human IgG1 Fc tag at the C-terminus.
GeneID 2324
Accession P35916-1
PredictedSize 110.5 kDa
SDS-PAGE 125-150 kDa, 85-95 kDa, 65-75kDa, reducing (R) conditions
Formulation Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally 5% trehalose and 5% mannitol are added as protectants before lyophilization.
Reconstitution Briefly centrifuge the tube before opening. Reconstitute at 0.1-0.5 mg/mL in sterile water.
Storage Conditions
It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
  • Until expiry date, -20℃ to -80℃ as lyophilized proteins.
  • 3 months, -20℃ to -80℃ under sterile conditions after reconstitution.
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the recommended temperature.

Background

FLT4 (Fms-related tyrosine kinase 4; also known as VEGFR3) is the main receptor for VEGFC (vascular endothelial growth factor C), and its activation mediates LEC (lymphatic endothelial cell) proliferation, migration, and surviva. FLT4 and the ligand VEGFC increase their expression in macrophages upon bacterial infection. Studies have demonstrated the critical roles of the FLT4-mediated pathway in the regulation of lymphatic and blood vascular development. FLT4 and its ligand VEGFC are expressed in leukemic blasts in AML and that the role of this signaling axis is closely related to blast survival. In addition, VEGFC and FLT4 are expressed in the BM (bone marrow) of AML (Acute myeloid leukemia) and VEGFC can protect AML blasts against chemotherapy by inducing their proliferation, showing the importance of VEGFC signaling in blast maintenance.

References:

1.Tuomas Tammela. et al. (2008). Nature. 454(7204):656-660. 2.Ayelet Jerafi-Vider. et al. (2021). Cell Reports. 35(11):109255. 3.Li Ma. et al. (2022). Autophagy.18(6):1385-1400. 4.de Jonge HJ. et al. (2008). Clinical Cancer Research. 14(3):924-930. 5.Sergio Dias. et al. (2002). Blood. 99(6):2179-2184.

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