EphA1 Double Nickase Plasmid (h): sc-403340-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EphA1 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
- EphA1 Double Nickase Plasmid (h) and EphA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EPHA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: EphA1 Antibody (5D2A4): sc-65993
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EphA1 Double Nickase Plasmid (h) | sc-403340-NIC | 20 µg | $410.00 | |||
EphA1 Double Nickase Plasmid (h2) | sc-403340-NIC-2 | 20 µg | $410.00 |
EPHA1 encodes EphA1, a receptor tyrosine kinase in the ephrin signaling network that mediates contact-dependent cell communication. EphA1 regulates cytoskeletal dynamics, cell adhesion, and directional migration through downstream pathways including Rho family GTPases, MAPK/ERK signaling, and PI3K-associated signaling outputs. In epithelial and endothelial contexts, EphA1 contributes to tissue boundary formation and cell–cell junction organization, linking altered receptor activity to changes in invasiveness and microenvironmental interactions. Dysregulated EPHA1 expression or signaling has been reported in multiple cancer types and is also studied in relation to neurobiology and inflammation-associated remodeling processes.
EphA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EPHA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EPHA1. 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 EPHA1 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 EPHA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.