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.
TRAP Double Nickase Plasmid (h): sc-400892-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAP 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
- TRAP Double Nickase Plasmid (h) and TRAP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACP5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRAP Antibody (D-3): sc-376875
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAP Double Nickase Plasmid (h) | sc-400892-NIC | 20 µg | $410.00 | |||
TRAP Double Nickase Plasmid (h2) | sc-400892-NIC-2 | 20 µg | $410.00 |
ACP5 encodes tartrate-resistant acid phosphatase (TRAP), a metalloenzyme enriched in osteoclasts and activated macrophages that hydrolyzes phosphate esters in acidic compartments. TRAP contributes to bone matrix remodeling, vesicular trafficking, and redox-related processes through dephosphorylation of extracellular and endosomal substrates, aligning with osteoclast differentiation programs downstream of RANKL–NF-κB and MAPK signaling. Altered ACP5/TRAP activity is linked to dysregulated bone turnover and inflammatory phenotypes, and it is frequently studied in the context of osteolytic disease mechanisms and immune cell activation states. In human cell models, ACP5 serves as a functional marker and mechanistic node for interrogating osteoclastogenesis, lysosomal biology, and macrophage polarization pathways.
TRAP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACP5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACP5. 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 ACP5 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 ACP5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.