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.
RANKL Double Nickase Plasmid (h): sc-400304-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RANKL 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
- RANKL Double Nickase Plasmid (h) and RANKL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TNFSF11. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RANKL Antibody (G-1): sc-377079
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RANKL Double Nickase Plasmid (h) | sc-400304-NIC | 20 µg | $410.00 | |||
RANKL Double Nickase Plasmid (h2) | sc-400304-NIC-2 | 20 µg | $410.00 |
TNFSF11 encodes receptor activator of NF-κB ligand (RANKL), a type II transmembrane and soluble cytokine of the TNF superfamily that signals through TNFRSF11A/RANK to regulate osteoclast differentiation, activation, and survival. RANKL–RANK engagement triggers canonical and noncanonical NF-κB signaling as well as MAPK and NFATc1-driven transcriptional programs, coordinating bone remodeling and coupling to immune cell function. Dysregulated RANKL signaling is strongly associated with inflammatory osteolysis and bone loss processes, including osteoporosis and rheumatoid arthritis–linked joint erosion, and contributes to tumor-associated osteolytic microenvironments. Because RANKL also shapes dendritic cell–T cell interactions and tissue-specific remodeling, TNFSF11 is widely studied in osteoimmunology and skeletal biology models.
RANKL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TNFSF11 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TNFSF11. 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 TNFSF11 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 TNFSF11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.