Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
OPG/Osteoprotegerin Double Nickase Plasmid (h): sc-400497-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OPG/Osteoprotegerin 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
- OPG/Osteoprotegerin Double Nickase Plasmid (h) and OPG/Osteoprotegerin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TNFRSF11B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: OPG/Osteoprotegerin Antibody (E-10): sc-390518
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OPG/Osteoprotegerin Double Nickase Plasmid (h) | sc-400497-NIC | 20 µg | $410.00 | |||
OPG/Osteoprotegerin Double Nickase Plasmid (h2) | sc-400497-NIC-2 | 20 µg | $410.00 |
TNFRSF11B encodes osteoprotegerin (OPG), a secreted decoy receptor in the TNF receptor superfamily that binds RANKL (TNFSF11) and TRAIL (TNFSF10), thereby modulating ligand availability and downstream signaling. By antagonizing RANK–RANKL interactions, OPG regulates osteoclast differentiation and activity, integrating with NF-κB and MAPK pathway outputs that control bone remodeling and immune crosstalk. Beyond skeletal biology, OPG is implicated in vascular calcification and endothelial–smooth muscle signaling, reflecting its role at the interface of inflammation and tissue homeostasis. Dysregulated TNFRSF11B expression or altered OPG/RANKL balance has been associated with bone density phenotypes, osteolytic processes, and calcific vascular disease mechanisms relevant to translational research.
OPG/Osteoprotegerin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TNFRSF11B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TNFRSF11B. 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 TNFRSF11B 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 TNFRSF11B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.