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Validated All-in-One™ qPCR Primer for FLT4(NM_182925.3) Search again
Product ID:
HQP005916
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CHTD7, FLT-4, FLT41, LMPH1A, LMPHM1, PCL, VEGFR-3, VEGFR3
Gene Description:
fms related receptor tyrosine kinase 4
Target Gene Accession:
NM_182925.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a tyrosine kinase receptor for vascular endothelial growth factors C and D. The protein is thought to be involved in lymphangiogenesis and maintenance of the lymphatic endothelium. Mutations in this gene cause hereditary lymphedema type IA. [provided by RefSeq].
Gene References into function
- A potential mechanism involved in hemangioma formation is the alteration of the FLT4 signaling pathway in endothelial and/or pericytic cells.
- VEGF-C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy.
- Suppression of tumor lymphangiogenesis and lymph node metastasis by blocking vascular endothelial growth factor receptor 3 signaling.
- Vascular endothelial growth factor receptor-3 (VEGFR-3) and its ligand VEGF-C are expressed in human colorectal adenocarcinoma.
- generation of endothelial cells from CD34+ cells is associated with expression of VEGFR3 on the cell surface
- Data demonstrate the expression of vascular endothelial growth factor receptor-3 and vascular endothelial growth factor-C on corneal dendritic cells, which implicate a potential relationship between lymphangiogenesis and leukocyte trafficking in the eye.
- the carboxyl-terminal tail of VEGFR-3 provides important regulatory tyrosine phosphorylation sites with potential signal transduction capacity and these sites are differentially used in ligand-induced homo- and heterodimeric receptor complexes
- Specific VEGFR3 expression, examined in 27 B-CLL samples, was positive in 26 of them. The VEGF transduction pathway may be very active in CLL cells. Both its paracrine & autocrine pathways may contribute to their enhanced survival.
- VEGF-C and its receptor FLT-4 play a role in the development of gastric cancer, and the tumors with expression of VEGF-C and FLT-4 are more likely to have lymph node metastasis.
- VEGFR-3 may protect against oxidative damage in endothelial cells, and that patients with hereditary lymphoedema may be susceptible to ROS-induced cell damage.
- expression levels were significantly elevated in primary prostatic tumors with sentinel lymph node involvement compared to those lacking lymph node involvement
- vascular endothelial growth factor receptor-3 may have a role in lymph node metastasis in prostate cancer
- integrin alpha5beta1 participates in the activation of both VEGFR-3 and its downstream PI3 kinase/Akt signaling pathway, which is essential for fibronectin-mediated lymphatic endothelial cell survival and proliferation.
- VEGFR-3 needs to be associated to VEGFR-2 to induce ligand-dependent cellular responses
- Patients with primary lymphedema have serum level of VEGF-D significantly higher than controls.The increased levels of VEGF-D suggest that primary lymphedema may be based on defective stimulation of VEGFR-3.
- Ang1 has a role in lymphatic vessel endothelial proliferation, Tie2 expression, and VEGFR-3 upregulation
- KSHV gB can activate VEGFR-3 on the microvascular endothelium and modulate endothelial cell migration and proliferation via an interaction between the alpha3beta1 integrin and the VEGFR-3 receptor
- increased expression of VEGF-C and VEGFR-3 play a role in prostate cancer progression and in metastasis to regional lymph nodes
- Overexpression of vascular endothelial growth factor receptor 3 is associated with lung adenocarcinoma
- VEGFR-3/flt4 was expressed in cancer stromal cells.
- VEGF-D/VEGFR-3 signaling plays a critical role in osteoblast maturation
- The VEGF-3/VEGFR-c ratio was positively associated with lymph node metastasis in non-small cell lung cancer .
- multiple myeloma cells (but not B-cell chronic lymphocytic leukemia cells) induced a dramatic increase in expression of VEGFR-1 and VEGFR-3 on human bone marrow endothelial cells
- These results suggest that the expression of VEGFRs and NRPs on keratinocytes may constitute important regulators for its activity and may possibly be responsible for the autocrine signaling in the epidermis.
- This is the first report of an exon 22 mutation of VEGFR3 in Milroy disease.
- VEGFR-3 may play a role in the abnormal endometrial angiogenesis of idiopathic menorrhagia.
- expression of VEGFR-3(S) is up-regulated in >75% of hepatitis B x antigen positive hepatocellular carcinoma (HCC) nodules; HBxAg may short circuit VEGFR-3(S) signaling in liver cancer
- Both VEGF-A and angiopoietin-2 upregulated the expression of VEGFR-3 in cultured lymphatic endothelial cells
- In non-small-cell lung cancer cells, VEGF-C/VEGFR-3 coexpression suggests an autocrine/paracrine loop responsible for a high proliferation rate in tumour cells.
- interaction of CEACAM1 with Prox1 and VEGFR-3 plays a crucial role in tumor lymphangiogenesis and reprogramming of vascular endothelial cells to lymphatic endothelial cells
- Expression of VEGF-C, VEGF-D and their receptor VEGFR-3 in diffuse large B-cell lymphomas.
- data suggest that VEGF-C alters lymphatic endothelial function through a mechanism involving VEGFR-3
- Data demonstrate that Notch1 and VEGFR-3 interact genetically, that Notch directly induces VEGFR-3 in blood endothelial cells to regulate vascular development, and that Notch and VEGF signaling may function in tumor lymphangiogenesis.
- Increased expression of VEGFR-3 is associated with acute myeloid leukaemia
- VEGFR-3 was expressed in malignant cells from different subtypes of MM
- VEGFR3 single nucleotide polymorphisms andthe haplotype GC in the VEGFA gene are associated with psoriasis in Koreans
- Three of the 4 Retiform hemangioendothelioma (RH) biopsies failed to demonstrate D2-40, none expressed VEGFR-3...RH is a vascular entity which usually does not have lymphatic differentiation, but may rarely express D2-40.
- The present study identified 2 novel VEGFR3 mutations in Japanese families with Milroy's disease.
- Under hypoxic conditions an autocrine loop between VEGF-C/VEGFR-3 and HIF-1 alpha is possible in breast carcinoma and lung carcinoma but not in colorectal carcinoma cell lines.
- Report expression of VEGF-C/VEGFR3 in osteosarcomas.
- VEGFR-3 expression is restricted to blood and lymphatic vessels in solid tumors.
- Provide further evidence that VEGF-C/VEGFR-3 are expressed and function in cancer cells.
- VEGF-C and VEGF-D expressions were associated with VEGFR-3 expression and were significantly correlated with both peritumoral lymphangiogenesis and lymph node metastasis.
- results implicate VEGFR-3 as a regulator of vascular network formation
- No association was detected between the Single Nucleotide Polymorphism in the Vascular Endothelial Growth Factor and susceptibility to hemifacial spasm.
- G933R and D1049N mutations in tyrosine kinase domains of FLT4 in Nonne-Milroy lymphadema
- VEGFR-1/-3 co-expression is associated with high hemoglobin level in childhood acute lymphoblastic leukemia
- prevalence of VEGFR3 mutations in patients with primary lymphoedema
- Reduced secretion of VEGF and expression of VEGF-R3 by placental endothelial cells in gestosis can be caused by functional deficiency of the endothelial cells and low viability of endothelial cells.