SerpinB1a Double Nickase Plasmid (m): sc-425896-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SerpinB1a 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
- SerpinB1a Double Nickase Plasmid (m) and SerpinB1a Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Serpinb1a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SerpinB1a Double Nickase Plasmid (m) | sc-425896-NIC | 20 µg | $410.00 | |||
SerpinB1a Double Nickase Plasmid (m2) | sc-425896-NIC-2 | 20 µg | $410.00 |
Serpinb1a encodes the serine protease inhibitor SerpinB1a, an intracellular clade B serpin that restrains neutrophil-derived proteases such as elastase, cathepsin G, and proteinase 3 to limit proteolytic damage during inflammation. By modulating protease-driven remodeling of extracellular matrix and regulating leukocyte survival, SerpinB1a influences innate immune signaling, stress responses, and tissue homeostasis. Altered SerpinB1a activity has been linked to dysregulated inflammatory phenotypes, susceptibility to infection-associated tissue injury, and impaired resolution of immune responses. In mouse models, Serpinb1a is therefore studied in pathways connecting granulocyte function, inflammatory proteostasis, and organ damage following acute or chronic inflammation.
SerpinB1a Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Serpinb1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Serpinb1a. 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 Serpinb1a 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 Serpinb1a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.