VEZF1 Double Nickase Plasmid (m): sc-423670-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VEZF1 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
- VEZF1 Double Nickase Plasmid (m) and VEZF1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Vezf1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEZF1 Double Nickase Plasmid (m) | sc-423670-NIC | 20 µg | $410.00 | |||
VEZF1 Double Nickase Plasmid (m2) | sc-423670-NIC-2 | 20 µg | $410.00 |
Vezf1 encodes VEZF1, a zinc finger DNA-binding transcription factor enriched in endothelial and hematopoietic contexts that helps coordinate vascular development and blood vessel patterning. VEZF1 regulates gene expression programs linked to angiogenesis, endothelial differentiation, and chromatin-associated transcriptional control, interfacing with pathways that shape vascular integrity and tissue perfusion. In mouse models, altered Vezf1 activity impacts vascular morphogenesis and embryonic viability, making it relevant for studying mechanisms underlying developmental vascular defects and endothelial dysfunction. Its transcriptional roles also support investigation of how vascular gene regulatory networks contribute to pathological neovascularization and inflammation-associated vascular remodeling in experimental disease settings.
VEZF1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Vezf1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Vezf1. 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 Vezf1 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 Vezf1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.