EphA1 Double Nickase Plasmid (m): sc-420191-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EphA1 Double Nickase Plasmid (m) 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 (m) and EphA1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Epha1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EphA1 Double Nickase Plasmid (m) | sc-420191-NIC | 20 µg | $410.00 | |||
EphA1 Double Nickase Plasmid (m2) | sc-420191-NIC-2 | 20 µg | $410.00 |
Mouse Epha1 encodes the receptor tyrosine kinase EphA1, a member of the Eph/ephrin signaling system that mediates contact-dependent communication between neighboring cells. EphA1 engagement regulates receptor clustering and tyrosine phosphorylation to control cytoskeletal remodeling, cell adhesion, and directional migration, influencing boundary formation and tissue patterning during development. Downstream signaling intersects with Rho family GTPases and MAPK/ERK-associated pathways that shape cell motility and growth responses. Dysregulated EphA1 activity has been linked to altered epithelial organization and invasion-related phenotypes, making Epha1 a useful locus for studying mechanisms relevant to tumor biology and microenvironmental interactions in mouse models.
EphA1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Epha1 locus in mouse 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.