Flt-1/VEGFR1 Double Nickase Plasmid (m): sc-420383-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Flt-1/VEGFR1 Double Nickase Plasmid (m) 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
- Flt-1/VEGFR1 Double Nickase Plasmid (m) and Flt-1/VEGFR1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Flt1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Flt-1/VEGFR1 Double Nickase Plasmid (m) | sc-420383-NIC | 20 µg | $410.00 | |||
Flt-1/VEGFR1 Double Nickase Plasmid (m2) | sc-420383-NIC-2 | 20 µg | $410.00 |
Flt1 encodes Flt-1/VEGFR1, a high-affinity receptor tyrosine kinase for VEGF-A, VEGF-B, and PlGF that regulates vascular development, endothelial cell migration, and permeability. In mouse tissues, VEGFR1 modulates VEGF signaling flux through PI3K–AKT, MAPK/ERK, and PLCγ-associated pathways, acting in both pro-angiogenic signaling and ligand sequestration depending on receptor isoforms and cellular context. Flt1 activity influences vascular patterning, inflammatory cell recruitment, and tissue remodeling, linking it to models of pathological angiogenesis, ischemia-associated neovascular responses, and tumor microenvironment vascularization. Altered VEGFR1 signaling is also relevant to studies of retinopathy and developmental vascular defects where VEGF pathway balance is critical.
Flt-1/VEGFR1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Flt1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Flt1. 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 Flt1 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 Flt1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.