V9134
Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-2 antibody produced in mouse
clone KDR-1, ascites fluid
Synonym(s):
Anti-KDR, Anti-VEGF R-2
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About This Item
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biological source
mouse
conjugate
unconjugated
antibody form
ascites fluid
antibody product type
primary antibodies
clone
KDR-1, monoclonal
contains
15 mM sodium azide
species reactivity
human
technique(s)
immunohistochemistry (frozen sections): 1:800 using human placenta
indirect ELISA: suitable
isotype
IgG1
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... KDR(3791)
General description
Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-2 (mouse IgG1 isotype) is derived from the KDR-1 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from an immunized mouse. Vascular endothelial growth factor (VEGF), is a homodimeric heparin-binding glycoprotein. It is a member of a family of endothelial cell mitogenic and angiogenic factors. The VEGFR2 gene has been mapped to human chromosome 4q11-q12, which is the same locus for PDGF receptor and c-kit.
The antibody reacts specifically with VEGF receptor 2 (KDR) and does not recognize VEGF receptor-1 (Flt1 receptor), VEGF receptor 3 (sFlt4), and PDGF-Rβ.
Immunogen
recombinant human extracellular domain of VEGFR-2 (KDR).
Application
Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-2 antibody produced in mouse has been used in:
- immunohistochemistry
- histology
- immunostaining
- enzyme linked immunosorbent assay (ELISA)
Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-2 antibody produced in mouse was used for FACS analysis of HUVECs.
Biochem/physiol Actions
Vascular endothelial growth factor (VEGF) specifically stimulates the proliferation of endothelial cells isolated from both small and large vessels. These include endothelial cells from adrenal cortex, cerebral cortex, fetal and adult aorta and human umbilical vein.
Vascular endothelial growth factors receptors (VEGF Rs) are receptor tyrosine kinases that bind to VEGF. VEGF plays an important role in embryonic vasculogenesis, angiogenesis and homeostasis. The binding of VEGF to VEGF R2 results in activation of MAPK, PI3K, PKC, FAK and Src kinase pathways. The biological roles of VEGF R2 include in epithelial cell growth, proliferation, survival, migration, vascular permeability and angiogenesis.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Vascular endothelial growth factor (VEGF) is an autocrine growth factor for VEGF receptor-positive human tumors
Masood R, et al.
Blood, 98(6), 1904-1913 (2001)
Axitinib affects cell viability and migration of a primary foetal lung adenocarcinoma culture
Menna C, et al.
Cancer Investigation, 32(1), 13-21 (2014)
Neuropilin-1 promotes VEGFR-2 trafficking through Rab11 vesicles thereby specifying signal output
Ballmer-Hofer K, et al.
Blood, 118(3), 816-826 (2011)
Chie-Pein Chen et al.
Stem cells (Dayton, Ohio), 26(2), 550-561 (2007-11-03)
Maternal cells can become engrafted in various fetal organs during pregnancy. The nature of the cells and the mechanisms of maternofetal cell trafficking are not clear. We demonstrate that human lineage-negative, CD34-negative (Lin(-)CD34(-)) multipotent mesenchymal stromal cells express alpha(2), alpha(4)
Markus Meissner et al.
Circulation research, 94(3), 324-332 (2003-12-20)
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors, originally implicated in the regulation of lipid and glucose homeostasis. In addition, natural and synthetic PPAR activators may control inflammatory processes by inhibition of distinct proinflammatory genes. As signaling via the vascular
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