Epiregulin Double Nickase Plasmid (h): sc-404273-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Epiregulin 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
- Epiregulin Double Nickase Plasmid (h) and Epiregulin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EREG. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Epiregulin Double Nickase Plasmid (h) | sc-404273-NIC | 20 µg | $410.00 | |||
Epiregulin Double Nickase Plasmid (h2) | sc-404273-NIC-2 | 20 µg | $410.00 |
EREG encodes epiregulin, a secreted EGF family ligand that activates EGFR/ERBB signaling to regulate epithelial and stromal cell proliferation, migration, and differentiation. Epiregulin engagement of receptor tyrosine kinases promotes downstream MAPK/ERK and PI3K/AKT pathway activity, influencing cell-cycle progression and survival programs. Aberrant EREG expression has been associated with dysregulated inflammatory responses, wound repair phenotypes, and oncogenic signaling contexts where EGFR pathway remodeling contributes to tumor growth, invasion, and microenvironmental crosstalk. As a ligand-level modulator of ERBB network output, EREG is frequently studied in models of epithelial biology, cytokine-driven signaling, and cancer-associated pathway dependencies.
Epiregulin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EREG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EREG. 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 EREG 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 EREG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.