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The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|Rat KDR ORF mammalian expression plasmid, C-GFPSpark tag||RG80113-ACG|
|Rat KDR ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80113-ACR|
|Rat KDR ORF mammalian expression plasmid, C-Flag tag||RG80113-CF|
|Rat KDR ORF mammalian expression plasmid, C-His tag||RG80113-CH|
|Rat KDR ORF mammalian expression plasmid, C-Myc tag||RG80113-CM|
|Rat KDR ORF mammalian expression plasmid, C-HA tag||RG80113-CY|
|Rat KDR ORF mammalian expression plasmid, N-Flag tag||RG80113-NF|
|Rat KDR ORF mammalian expression plasmid, N-His tag||RG80113-NH|
|Rat KDR ORF mammalian expression plasmid, N-Myc tag||RG80113-NM|
|Rat KDR ORF mammalian expression plasmid, N-HA tag||RG80113-NY|
|Rat KDR natural ORF mammalian expression plasmid||RG80113-UT|
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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.