VEGF Double Nickase Plasmid (r): sc-437276-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VEGF Double Nickase Plasmid (r) 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
- VEGF Double Nickase Plasmid (r) and VEGF Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: VEGF Antibody (C-1): sc-7269
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEGF Double Nickase Plasmid (r) | sc-437276-NIC | 20 µg | $410.00 | |||
VEGF Double Nickase Plasmid (r2) | sc-437276-NIC-2 | 20 µg | $410.00 |
Vascular endothelial growth factor (VEGF) is a secreted signaling protein that coordinates endothelial cell proliferation, migration, and survival to regulate angiogenesis and vascular permeability. Through VEGFR1/VEGFR2 receptor tyrosine kinase signaling, VEGF engages PI3K–AKT, MAPK/ERK, PLCγ–PKC, and eNOS pathways, integrating cues from hypoxia-driven HIF-1 signaling and extracellular matrix remodeling. Altered VEGF activity is linked to pathological neovascularization, edema, and inflammatory vascular dysfunction in models of retinal disease, ischemic injury, tumor microenvironments, and chronic wound repair. In rat systems, VEGF perturbation is commonly used to interrogate vessel patterning, blood–tissue barrier integrity, and neurovascular coupling.
VEGF Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.