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.
Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h): sc-400564-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Endothelin-1/EDN1/ET-1 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
- Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h) and Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EDN1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Endothelin-1/EDN1/ET-1 Antibody (C7): sc-517436
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h) | sc-400564-NIC | 20 µg | $410.00 | |||
Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h2) | sc-400564-NIC-2 | 20 µg | $410.00 |
EDN1 encodes endothelin-1 (ET-1), a potent secreted vasoactive peptide produced by endothelial and other cell types that regulates vascular tone, smooth muscle contraction, and mitogenic responses. ET-1 signals primarily through endothelin receptors (EDNRA/EDNRB) to activate G protein–coupled pathways including PLCβ–IP3/Ca²⁺, PKC, MAPK/ERK, and RhoA/ROCK, shaping vasoreactivity, inflammation, and extracellular matrix remodeling. Dysregulated EDN1 expression and signaling are studied in contexts of endothelial dysfunction, hypoxia responses, and fibrotic and hypertrophic remodeling programs. Altered ET-1 axis activity has been implicated in cardiopulmonary and renal pathophysiology and is frequently examined as a mediator of vascular inflammation and tissue remodeling in disease-relevant models.
Endothelin-1/EDN1/ET-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EDN1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EDN1. 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 EDN1 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 EDN1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.