RECK Double Nickase Plasmid (h): sc-402440-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RECK 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
- RECK Double Nickase Plasmid (h) and RECK Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RECK. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RECK Antibody (G-4): sc-373929
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RECK Double Nickase Plasmid (h) | sc-402440-NIC | 20 µg | $410.00 | |||
RECK Double Nickase Plasmid (h2) | sc-402440-NIC-2 | 20 µg | $410.00 |
RECK (reversion-inducing cysteine-rich protein with Kazal motifs) is a membrane-anchored regulator of extracellular matrix remodeling that suppresses the activity of multiple matrix metalloproteinases, including MMP2, MMP9, and MT1-MMP/MMP14. By restraining pericellular proteolysis, RECK influences cell–matrix adhesion, migration, and invasive behavior, and contributes to vascular and tissue morphogenesis. RECK function intersects with pathways governing epithelial–mesenchymal dynamics and protease-driven signaling in the tumor microenvironment. Reduced RECK expression or dysregulated RECK–MMP balance has been associated with increased matrix degradation in several cancer contexts and other pathologies characterized by aberrant remodeling.
RECK Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RECK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RECK. 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 RECK 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 RECK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.