p20-ARC Double Nickase Plasmid (m): sc-426917-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p20-ARC 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
- p20-ARC Double Nickase Plasmid (m) and p20-ARC Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Arpc4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p20-ARC Double Nickase Plasmid (m) | sc-426917-NIC | 20 µg | $410.00 |
Mouse Arpc4 encodes p20-ARC, an essential subunit of the Arp2/3 complex that drives actin filament nucleation and branching to generate dynamic cortical actin networks. Through coordinated regulation by nucleation-promoting factors such as WASP/WAVE downstream of Rho-family GTPases, p20-ARC supports lamellipodia formation, endocytosis, vesicle trafficking, and phagocytosis, shaping cell polarity and motility. Disruption of Arp2/3-dependent actin remodeling is linked to altered immune cell function, impaired tissue morphogenesis, and invasive behaviors in disease-relevant cellular models, making Arpc4 a core node for cytoskeletal pathway interrogation.
p20-ARC Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Arpc4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Arpc4. 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 Arpc4 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 Arpc4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.