ER71 Double Nickase Plasmid (h): sc-404462-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ER71 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
- ER71 Double Nickase Plasmid (h) and ER71 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ETV2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ER71 Double Nickase Plasmid (h) | sc-404462-NIC | 20 µg | $410.00 | |||
ER71 Double Nickase Plasmid (h2) | sc-404462-NIC-2 | 20 µg | $410.00 |
Human ETV2 encodes the ETS transcription factor ER71, a master regulator of vascular and hematopoietic lineage specification during early development. ER71 binds ETS motifs to activate endothelial gene programs, driving processes such as vasculogenesis, angiogenic sprouting, and endothelial-to-hematopoietic transitions through pathways that interface with VEGF/VEGFR signaling and broader transcriptional networks controlling vascular identity. Dysregulated ETV2/ER71 activity has been associated with abnormal endothelial differentiation and vascular remodeling phenotypes, making it relevant to studies of developmental biology, tissue vascularization, and tumor-associated angiogenesis. Because ER71 sits near the top of endothelial transcriptional hierarchies, perturbing ETV2 provides a direct entry point to map downstream gene networks and lineage decisions.
ER71 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ETV2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ETV2. 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 ETV2 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 ETV2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.