EFR3A Double Nickase Plasmid (m): sc-429403-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EFR3A 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
- EFR3A Double Nickase Plasmid (m) and EFR3A Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Efr3a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EFR3A Double Nickase Plasmid (m) | sc-429403-NIC | 20 µg | $410.00 | |||
EFR3A Double Nickase Plasmid (m2) | sc-429403-NIC-2 | 20 µg | $410.00 |
Mouse Efr3a encodes EFR3A, a conserved plasma membrane–associated scaffold that helps recruit phosphatidylinositol 4-kinase activity to the cell surface, supporting phosphoinositide homeostasis and downstream signaling. Through regulation of PI4P and related phosphoinositide pools, EFR3A influences membrane trafficking, receptor signaling, and actin-dependent processes that shape cell polarity and adhesion. This pathway is central to dynamic control of membrane identity and phosphoinositide-dependent signaling networks used broadly across tissues, including the nervous system. Perturbation of phosphoinositide metabolism is implicated in multiple disorders, making Efr3a a useful target for mechanistic studies of membrane signaling and cellular organization in mouse models.
EFR3A Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Efr3a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Efr3a. 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 Efr3a 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 Efr3a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.