ADAM10 Double Nickase Plasmid (h): sc-400883-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAM10 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
- ADAM10 Double Nickase Plasmid (h) and ADAM10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADAM10. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ADAM10 Antibody (B-3): sc-28358
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAM10 Double Nickase Plasmid (h) | sc-400883-NIC | 20 µg | $410.00 | |||
ADAM10 Double Nickase Plasmid (h2) | sc-400883-NIC-2 | 20 µg | $410.00 |
ADAM10 encodes a zinc-dependent transmembrane metalloprotease of the ADAM family that mediates ectodomain shedding of diverse cell-surface proteins, thereby remodeling receptor availability and cell–cell communication. ADAM10 participates in regulated intramembrane proteolysis and influences Notch signaling, APP processing, and cleavage of adhesion and immune modulatory molecules such as cadherins, ligands, and cytokine receptors. Through these activities it affects neuronal development, synaptic function, epithelial barrier biology, and immune responses, integrating cues across membrane-proximal signaling networks. Dysregulated ADAM10 activity or expression has been implicated in cancer-associated signaling and invasion phenotypes, neurodegenerative mechanisms linked to APP metabolism, and inflammatory pathophysiology, supporting its value as a mechanistic target in pathway studies.
ADAM10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADAM10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADAM10. 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 ADAM10 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 ADAM10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.