β-Amyloid Double Nickase Plasmid (h): sc-400520-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β-Amyloid 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
- β-Amyloid Double Nickase Plasmid (h) and β-Amyloid Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: β-Amyloid Antibody (6C3): sc-517461
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β-Amyloid Double Nickase Plasmid (h) | sc-400520-NIC | 20 µg | $410.00 | |||
β-Amyloid Double Nickase Plasmid (h2) | sc-400520-NIC-2 | 20 µg | $410.00 |
APP encodes amyloid precursor protein, a type I transmembrane glycoprotein broadly expressed in neurons and other tissues and processed through regulated secretory trafficking. Sequential cleavage by α-, β-, and γ-secretases generates multiple peptides, including β-Amyloid, linking APP metabolism to endosomal–lysosomal function, synaptic activity, and membrane lipid homeostasis. β-Amyloid is implicated in protein aggregation and cellular stress responses that intersect with neuroinflammatory signaling, oxidative injury pathways, and altered neuronal connectivity. Dysregulated APP processing and β-Amyloid accumulation are central molecular features studied in neurodegeneration and related proteostasis disorders.
β-Amyloid Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APP. 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 APP 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 APP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.