RADIL Double Nickase Plasmid (h): sc-407813-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RADIL 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
- RADIL Double Nickase Plasmid (h) and RADIL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RADIL. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RADIL Double Nickase Plasmid (h) | sc-407813-NIC | 20 µg | $410.00 |
RADIL (Ras association and dilute domain containing) encodes a cytoplasmic adaptor that links activated small GTPase signaling to cytoskeletal remodeling and cell motility. RADIL participates in integrin-dependent adhesion, focal adhesion dynamics, and directed migration by coordinating signaling inputs that regulate actin organization and cell polarity. Through these functions it is studied in processes such as vascular and immune cell trafficking, epithelial morphogenesis, and invasive migration programs relevant to cancer biology. Dysregulated RADIL-associated migration pathways have been connected to altered metastatic potential and changes in cell–matrix interactions in multiple experimental systems.
RADIL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RADIL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RADIL. 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 RADIL 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 RADIL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.