Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h): sc-400118-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h) and Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KDR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Flk-1/KDR/VEGFR2 Antibody (D-8): sc-393163
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h) | sc-400118-NIC | 20 µg | $410.00 | |||
Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h2) | sc-400118-NIC-2 | 20 µg | $410.00 |
KDR encodes the receptor tyrosine kinase Flk-1/KDR/VEGFR2, a principal signaling receptor for VEGF ligands in vascular endothelial cells. Ligand-induced dimerization and autophosphorylation activates PI3K–AKT, RAS–RAF–MEK–ERK, PLCγ–PKC, and SRC-family pathways to coordinate endothelial proliferation, migration, survival, and vascular permeability during angiogenesis and vasculogenesis. VEGFR2 signaling also interfaces with nitric oxide production and cytoskeletal remodeling programs that shape vessel maturation and sprouting. Dysregulated KDR activity and expression are widely studied in tumor angiogenesis, ischemia-associated neovascular responses, and inflammatory vascular remodeling.
Flk-1/KDR/VEGFR2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KDR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KDR. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt KDR function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of KDR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.