Serglycin Double Nickase Plasmid (m): sc-422394-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Serglycin 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
- Serglycin Double Nickase Plasmid (m) and Serglycin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Srgn. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Serglycin Antibody (C-11): sc-374657
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Serglycin Double Nickase Plasmid (m) | sc-422394-NIC | 20 µg | $410.00 |
Mouse Srgn encodes serglycin, a secreted and granule-associated proteoglycan that carries chondroitin sulfate chains to package and stabilize cationic mediators such as proteases, chemokines, and antimicrobial peptides. Serglycin contributes to regulated exocytosis and extracellular matrix remodeling, influencing immune cell degranulation, inflammatory signaling, and cell–cell communication. In hematopoietic and myeloid lineages, it supports granule biogenesis and storage of effector molecules that shape innate and adaptive immune responses. Altered serglycin expression or glycosaminoglycan composition has been linked to dysregulated inflammation and tumor-associated microenvironment processes, making Srgn a useful node for mechanistic studies of immune modulation and protease-dependent pathways.
Serglycin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Srgn locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Srgn. 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 Srgn 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 Srgn-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.