EphA7 Double Nickase Plasmid (h): sc-401722-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EphA7 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
- EphA7 Double Nickase Plasmid (h) and EphA7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EPHA7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: EphA7 Antibody (E-7): sc-393973
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EphA7 Double Nickase Plasmid (h) | sc-401722-NIC | 20 µg | $410.00 | |||
EphA7 Double Nickase Plasmid (h2) | sc-401722-NIC-2 | 20 µg | $410.00 |
EPHA7 encodes EphA7, a receptor tyrosine kinase of the ephrin (Eph) family that mediates cell–cell communication through binding to membrane-tethered ephrin-A ligands. EphA7 signaling coordinates axon guidance, neuronal and cortical patterning, and tissue boundary formation by regulating cytoskeletal remodeling, adhesion, and directional migration. Downstream effects intersect with Rho family GTPase signaling and kinase cascades that influence proliferation and differentiation programs. Dysregulated EPHA7 activity and altered ephrin/Eph pathway balance have been reported in multiple disease contexts, including neurodevelopmental disorders and cancer-associated changes in invasion and cell sorting.
EphA7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EPHA7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EPHA7. 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 EPHA7 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 EPHA7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.