Asporin Double Nickase Plasmid (m): sc-426152-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Asporin Double Nickase Plasmid (m) 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
- Asporin Double Nickase Plasmid (m) and Asporin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Aspn. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Asporin Double Nickase Plasmid (m) | sc-426152-NIC | 20 µg | $410.00 | |||
Asporin Double Nickase Plasmid (m2) | sc-426152-NIC-2 | 20 µg | $410.00 |
Aspn encodes asporin, a small leucine-rich proteoglycan of the extracellular matrix that contributes to collagen fibrillogenesis and regulation of matrix organization in musculoskeletal tissues. Mouse asporin can modulate growth factor signaling, including interactions that influence TGF-β family pathways, thereby affecting chondrogenesis, osteogenesis, and fibrocartilaginous homeostasis. Altered ASPN expression or function has been linked to dysregulated extracellular matrix remodeling and inflammatory signaling, making it relevant to studies of osteoarthritis, intervertebral disc degeneration, tendon/ligament pathology, and fibrosis-associated matrix changes. In vitro and in vivo models often use Aspn perturbation to dissect how stromal matrix cues shape cell adhesion, mechanotransduction, and differentiation programs.
Asporin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Aspn locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Aspn. 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 Aspn 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 Aspn-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.