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AB134453

Recombinant mouse VEGF Receptor 2 protein

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Recombinant mouse VEGF Receptor 2 protein is a Mouse Fragment protein, in the 20 to 660 aa range, expressed in Insect cells, with >95%, suitable for SDS-PAGE, ELISA.

View Alternative Names

CD309, Flk-1, Flk1, Kdr, Vascular endothelial growth factor receptor 2, VEGFR-2, Fetal liver kinase 1, Kinase NYK, Protein-tyrosine kinase receptor flk-1, FLK-1

2 Images
Functional Studies - Recombinant mouse VEGF Receptor 2 protein (AB134453)
  • FuncS

Unknown

Functional Studies - Recombinant mouse VEGF Receptor 2 protein (AB134453)

Inhibition of the VEGF165-induced proliferation of HUVE cells by recombinant human and mouse endogenous sKDR and sFlk-1 HUVECs were stimulated with 10 ng/ml VEGF165, both soluble receptors were added with a 100X excess.

SDS-PAGE - Recombinant mouse VEGF Receptor 2 protein (AB134453)
  • SDS-PAGE

Unknown

SDS-PAGE - Recombinant mouse VEGF Receptor 2 protein (AB134453)

SDS-PAGE analysis of recombinant mouse soluble VEGFR-1 produced in insect cells. Sample was loaded in 10% SDS-polyacrylamide gel under reducing condition and stained with Coomassie blue.

Key facts

Purity

>95% SDS-PAGE

Expression system

Insect cells

Tags

Tag free

Applications

SDS-PAGE, ELISA

applications

Biologically active

Yes

Biological activity

ab134453 activity was measured by its ability to bind to immobilized recombinant Human VEGF165 in a functional ELISA.

Accession

P35918

Animal free

No

Carrier free

No

Species

Mouse

Reconstitution

Reconstitute in water or PBS

Storage buffer

Constituents: 0.58% Sodium chloride, 0.49% MES

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "ELISA": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

Product details

Store at 4°C for not longer than 2 days.

Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. A splice variant of the gene encoding vascular endothelial growth factor receptor-2 (VEGFR-2) that encodes a secreted form of the protein, designated endogenous soluble VEGFR-2 (esVEGFR-2/KDR) has been described. The endogenous soluble esKDR inhibits developmental and reparative lymphangiogenesis by blocking VEGF-C function. Tissue-specific loss of esKDR in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of esKDR inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring esKDR thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of esKDR might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema. Recombinant mouse esKDR generated by alternative splicing consist of the first 6 Ig-like loops followed by the unique C-terminal end: GMEASLGDRIAMP.

Sequence info

[{"sequence":"MESKALLAVALWFCVETRAASVGLTGDFLHPPKLSTQKDILTILANTTLQITCRGQRDLDWLWPNAQRDSEERVLVTECGGGDSIFCKTLTIPRVVGNDTGAYKCSYRDVDIASTVYVYVRDYRSPFIASVSDQHGIVYITENKNKTVVIPCRGSISNLNVSLCARYPEKRFVPDGNRISWDSEIGFTLPSYMISYAGMVFCEAKINDETYQSIMYIVVVVGYRIYDVILSPPHEIELSAGEKLVLNCTARTELNVGLDFTWHSPPSKSHHKKIVNRDVKPFPGTVAKMFLSTLTIESVTKSDQGEYTCVASSGRMIKRNRTFVRVHTKPFIAFGSGMKSLVEATVGSQVRIPVKYLSYPAPDIKWYRNGRPIESNYTMIVGDELTIMEVTERDAGNYTVILTNPISMEKQSHMVSLVVNVPPQIGEKALISPMDSYQYGTMQTLTCTVYANPPLHHIQWYWQLEEACSYRPGQTSPYACKEWRHVEDFQGGNKIEVTKNQYALIEGKNKTVSTLVIQAANVSALYKCEAINKAGRGERVISFHVIRGPEITVQPAAQPTEQESVSLLCTADRNTFENLTWYKLGSQATSVHMGESLTPVCKNLDALWKLNGTMFSNSTNDILIVAFQNASLQDQGDYVCSAQDKKTKKRHCLVKQLIILGMEASLGDRIAMP","proteinLength":"Fragment","predictedMolecularWeight":"105 kDa","actualMolecularWeight":null,"aminoAcidEnd":660,"aminoAcidStart":20,"nature":"Recombinant","expressionSystem":"Insect cells","accessionNumber":"P35918","tags":[]}]

Properties and storage information

Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
-80°C
Appropriate long-term storage conditions
-80°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle
True

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

VEGF Receptor 2 also known as KDR or Flk-1 is a receptor tyrosine kinase important for mediating the effects of vascular endothelial growth factor (VEGF). This protein has a mass of approximately 150 kDa. It mostly expresses in vascular endothelial cells playing a primary role in the formation of blood vessels. The receptor can also be found in various non-endothelial tissues though in smaller amounts indicating its broad functional roles outside of the vascular system.
Biological function summary

VEGF Receptor 2 is important for angiogenesis and vascular permeability. It is part of the VEGF receptor family which also includes VEGF Receptors 1 and 3 forming a complex interaction network. Upon binding with VEGF it phosphorylates key proteins to initiate signals that regulate endothelial cell migration proliferation and survival. The receptor's function is critical for normal developmental processes and wound healing as well.

Pathways

VEGF Receptor 2 is especially important within the angiogenesis and vascular permeability pathways. It plays a central role in the VEGF signaling pathway alongside proteins like VEGF A which is the primary ligand for the receptor. The signaling through this receptor modulates various downstream proteins through phosphorylation linking it to pathways that control cellular responses essential for blood vessel formation and maintenance.

VEGF Receptor 2 is significantly linked with cancer and age-related macular degeneration. In the context of cancer the overexpression or dysregulation of VEGF and its receptors including VEGF Receptor 2 often leads to enhanced tumor angiogenesis promoting tumor growth and metastasis. Additionally the receptor interacts with other proteins in pathological states such as CD309 in endothelial cell-based assays which are used for research like flow cytometry and ELISA to monitor VEGF Receptor 2 activity and its impact on diseases.

Specifications

Form

Lyophilized

Additional notes

ab134453 was determined to be > 95% pure by SDS-PAGE and silver stain. Endotoxin level:< 0.1 ng per ug of VEGF Receptor 2. Affinity purified.

General info

Function

Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFC and VEGFD. Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. Promotes proliferation, survival, migration and differentiation of endothelial cells. Promotes reorganization of the actin cytoskeleton. Isoforms lacking a transmembrane domain, such as isoform 2, may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Isoform 2 plays an important role as a negative regulator of VEGFA- and VEGFC-mediated lymphangiogenesis by limiting the amount of free VEGFA and/or VEGFC and by preventing their binding to FLT4. Modulates FLT1 and FLT4 signaling by forming heterodimers. Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, reorganization of the actin cytoskeleton and activation of PTK2/FAK1. Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. Phosphorylates PLCG1. Promotes phosphorylation of FYN, NCK1, NOS3, PIK3R1, PTK2/FAK1 and SRC.

Sequence similarities

Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily.

Post-translational modifications

N-glycosylated.. Ubiquitinated. Tyrosine phosphorylation of the receptor promotes its poly-ubiquitination, leading to its degradation via the proteasome or lysosomal proteases (By similarity).. 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-949 is important for interaction with SH2D2A/TSAD and VEGFA-mediated reorganization of the actin cytoskeleton. Phosphorylation at Tyr-1173 is important for interaction with PLCG1 and SHB. Phosphorylation at Tyr-1212 is important for interaction with NCK1 and FYN. Dephosphorylated by PTPRJ at Tyr-799, Tyr-949, Tyr-994, Tyr-1052, Tyr-1057, Tyr-1173 and Tyr-1212 (By similarity).. The inhibitory disulfide bond between Cys-1022 and Cys-1043 may serve as a specific molecular switch for H(2)S-induced modification that regulates KDR/VEGFR2 function.

Subcellular localisation

Nucleus

Product protocols

Target data

Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFC and VEGFD. Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. Promotes proliferation, survival, migration and differentiation of endothelial cells. Promotes reorganization of the actin cytoskeleton. Isoforms lacking a transmembrane domain, such as isoform 2, may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Isoform 2 plays an important role as a negative regulator of VEGFA- and VEGFC-mediated lymphangiogenesis by limiting the amount of free VEGFA and/or VEGFC and by preventing their binding to FLT4. Modulates FLT1 and FLT4 signaling by forming heterodimers. Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, reorganization of the actin cytoskeleton and activation of PTK2/FAK1. Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. Phosphorylates PLCG1. Promotes phosphorylation of FYN, NCK1, NOS3, PIK3R1, PTK2/FAK1 and SRC.
See full target information Kdr

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