|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A myc tag can be used in many different assays that require recognition by an antibody. If there is no antibody against the studied protein, adding a myc-tag allows one to follow the protein with an antibody against the Myc epitope. Examples are cellular localization studies by immunofluorescence or detection by Western blotting.
The peptide sequence of the myc-tag is: N-EQKLISEEDL-C (1202 Da). It can be fused to the C-terminus and the N-terminus of a protein. It is advisable not to fuse the tag directly behind the signal peptide of a secretory protein, since it can interfere with translocation into the secretory pathway.
|Mouse KDR ORF mammalian expression plasmid, C-GFPSpark tag||MG50998-ACG|
|Mouse KDR ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50998-ACR|
|Mouse KDR ORF mammalian expression plasmid, C-Flag tag||MG50998-CF|
|Mouse KDR ORF mammalian expression plasmid, C-His tag||MG50998-CH|
|Mouse KDR ORF mammalian expression plasmid, C-Myc tag||MG50998-CM|
|Mouse KDR ORF mammalian expression plasmid, C-HA tag||MG50998-CY|
|Mouse KDR Gene cDNA clone plasmid||MG50998-G|
|Mouse KDR ORF mammalian expression plasmid, N-Flag tag||MG50998-NF|
|Mouse KDR ORF mammalian expression plasmid, N-His tag||MG50998-NH|
|Mouse KDR ORF mammalian expression plasmid, N-Myc tag||MG50998-NM|
|Mouse KDR ORF mammalian expression plasmid, N-HA tag||MG50998-NY|
|Mouse KDR natural ORF mammalian expression plasmid||MG50998-UT|
|Learn more about expression Vectors|
VEGFR2, also called as KDR or Flk-1, is identified as the receptor for VEGF and VEGFC and an early marker for endothelial cell progenitors, whose expression is restricted to endothelial cells in vivo. VEGFR2 was shown to be the primary signal transducer for angiogenesis and the development of pathological conditions such as cancer and diabetic retinopathy. It has been shown that VEGFR2 is expressed mainly in the endothelial cells, and the expression is upregulated in the tumor vasculature. Thus the inhibition of VEGFR2 activity and its downstream signaling are important targets for the treatment of diseases involving angiogenesis. VEGFR2 transduces the major signals for angiogenesis via its strong tyrosine kinase activity. However, unlike other representative tyrosine kinase receptors, VEGFR2 does not use the Ras pathway as a major downstream signaling but rather uses the phospholipase C-protein kinase C pathway to signal mitogen-activated protein (MAP)-kinase activation and DNA synthesis. VEGFR2 is a direct and major signal transducer for pathological angiogenesis, including cancer and diabetic retinopathy, in cooperation with many other signaling partners; thus, VEGFR2 and its downstream signaling appear to be critical targets for the suppression of these diseases. VEGF and VEGFR2-mediated survival signaling is critical to endothelial cell survival, maintenance of the vasculature and alveolar structure and regeneration of lung tissue. Reduced VEGF and VEGFR2 expression in emphysematous lungs has been linked to increased endothelial cell death and vascular regression.