Soluble VEGF R2 (sVEGFR2)ELISA Soluble VEGF R3 (sVEGFR3)ELISA |
| Biomarker for Cardiovascular Disease and Tumor |
Alternative name:
- Protein-tyrosine kinase receptor flk-1
- Fetal liver kinase 1
- CD_antigen=CD309
- VEGF-R2
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Receptor for VEGF, VEGFB and PGF. Has a tyrosine-protein kinase activity. The VEGF-kinase ligand/receptor signaling system plays a key role in vascular development and regulation of vascular permeability. Isoform SFlt1 may have an inhibitory role in angiogenesis. |
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| Soluble VEGFR-2: an antilymphangiogenic variant of VEGF receptors |
| The vascular endothelial growth factor (VEGF) family of secreted proteins and their receptors are major regulators of blood vessel development (hemangiogenesis) and lymphatic vessel development (lymphangiogenesis). VEGF acts through a complex system of receptor tyrosine kinases, which can be membrane bound or soluble. New data concerning the receptor system are still emerging, thus contributing to the complexity of the system. Very recently a soluble form of VEGFR-2, termed sVEGFR-2, which is a result of alternative splicing, has been discovered. Earlier, it has been shown that a secreted/soluble form of VEGFR-1, termed sVEGFR-1, is produced by alternative splicing and exerts an antihemangiogenic effect by binding VEGF-A. The newly discovered spliced variant of sVEGFR-2 binds the lymphangiogenic growth factor VEGF-C and thus inhibits VEGF-C-induced activation of VEGFR-3, consequently inhibiting lymphatic endothelial cell proliferation. Its inactivation in murine embryos permits hyperplasia of dermal lymphatics and invasion of lymphatics into the cornea. Tumor lymphangiogenesis seems to influence the metastatic behavior of malignant cells. A correlation has been found between the downregulation of sVEGFR-2 and the malignant progression of neuroblastoma, which is characterized by lymphogenic metastases in progressed stages. Data show that lymphangiogenesis is regulated by both activators and inhibitors, and its balance is crucial in health and disease. |
| Pavlakovic H,, et al. .Ann N Y Acad Sci. 2010 Oct;1207 Suppl 1:E7-15. doi: 10.1111/j.1749-6632.2010.05714.x. |
Presence of VEGF-R3 in the serum of metastatic malignant melanoma patients: Relationship with clinicobiological parameters. |
| The presence of metastases is a strong indicator of poor survival in many types of cancer. It has recently been shown that vascular endothelial growth factor-C (VEGF-C), and its receptor Flt-4 (VEGF-R3) are increased in a variety of tumours and may play a pivotal role in the promotion of metastasis. We previously demonstrated that high soluble VEGF-C level was correlated to high tumor burden. Objectives: This study was designed to i) detect and evaluate whether soluble VEGF-R3 play a role in metastatic malignant melanoma patients ii) to determine if they have any relationship with clinicobiological parameters, clinical response and survivals. Methods and Patients: using a sensitive enzyme-linked immunosorbent assays, VEGF-R3 was retrospectively measured in sera of 60 patients with a fully documented history of melanoma disease in comparison with 30 healthy controls. Disease free survival (DFS) and overall survival (OS) were calculated from the beginning of treatment until either the progression (DFS) or death (OS) and analyzed using the Kaplan-Meier method. Results: Pretreatment circulating VEGF-R3 was detectable in all samples from either melanoma patients or healthy donors. Furthermore, median level of sVEGF-R3 was significantly higher (p = 0.000015) in melanoma patients as compared to healthy donors. (38890 vs 30773 pg/ml respectively). No significant association was noted between sVEGF-R3 levels and gender, age or LDH level. Median serum VEGF-R3 level was significantly higher in patients with high tumor burden as compared to patients with low tumor burden (p = 0.045). The pretreatment sVEGF-R3 level was significantly different (p = 0.025) between responder (n = 27) and non-responding patients (n = 33). Lastly, the relapse-free survival was higher in the group with low sVEGF-R3 concentration compared to the high one's (14.1 vs 11,9 months) as well as for OS (14.3 Vs 12.6 months) but theses differences were not significant (ψ2 = 2,30, p = 0.12 & ψ2 = 0.74, p = 0.37 respectively). Conclusion: these results suggest that high pretreatment sVEGF-R3 level is related to bad prognosis in melanoma patients. |
| R. Mouawad, et al. Journal of Clinical Oncology, 2006 ASCO Annual Meeting Proceedings Part I. Vol 24, No. 18S (June 20 Supplement), 2006: 18004 |
| New Anti Human VEGFR2 Antibody A00123-02-100 for ICC-IF |
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Code No.: SK00123-06
Size: 96 T
Price: $460.00 USD
Standard Range:25-1600 pg/ml
Sensitivity:7.8 pg/ml
Sample Type: serum, EDTA plasma
Dolution Factor: 2-4
Sample requres: 25 ul
IntraCV: 6-8%
InterCV: 10-12%
Protocol: PDF |
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Code No.: SK00123-08
Size: 96 T
Price: $590.00 USD
Standard Range:31.25-2000 pg/ml
Sensitivity:7.8 pg/ml
Sample Type: serum, EDTA plasma
Dolution Factor: 2-4
Sample requres: 25 ul
IntraCV: 6-8%
InterCV: 10-12%
Protocol: PDF |
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| Name |
Code No. |
Size |
Price ($) |
| Soluble VEGF-R2 (Human) ELISA Kit |
|
96 T |
460.00 |
| Soluble VEGF-R2(Human) ELISA Kit |
|
96 T |
590.00 |
| Soluble VEGF-R2(Human) Rec (HEK293) |
00123-01-50 |
50 ug |
460.00 |
| Soluble VEGF-R2(Human) Rec (HEK293) |
00123-01-100 |
100 ug |
760.00 |
| Soluble VEGF-R2(Human) Rec (HEK293) |
00123-01-50B |
50 ug |
690.00 |
| Anti VEGF-R2(Human) IgG for ICC-IF and IHC |
A00123-02-50 |
50 ul |
320.00 |
| Anti VEGF-R2(Human) IgG for ICC-IF and IHC |
A00123-02-100 |
100 ul |
520.00 |
| Anti VEGF-R2(Human) IgG for ICC-IF and IHC |
A00123-03-50 |
50 ul |
269.00 |
| Anti VEGF-R2(Human) IgG for ICC-IF and IHC |
A00123-03-100 |
100 ul |
490.00 |