gasdermin Double Nickase Plasmid (h): sc-410658-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- gasdermin 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
- gasdermin Double Nickase Plasmid (h) and gasdermin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GSDMA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: gasdermin Antibody (H-6): sc-376318
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
gasdermin Double Nickase Plasmid (h) | sc-410658-NIC | 20 µg | $410.00 | |||
gasdermin Double Nickase Plasmid (h2) | sc-410658-NIC-2 | 20 µg | $410.00 |
Human GSDMA encodes gasdermin A, a member of the gasdermin family implicated in epithelial homeostasis and regulated cell death pathways linked to membrane permeabilization. Gasdermins are best known as downstream effectors of inflammasome-associated signaling and pyroptosis, shaping cytokine release and barrier inflammatory responses. GSDMA expression is enriched in stratified epithelia and has been associated with genetic and transcriptional programs relevant to asthma, inflammatory skin phenotypes, and other immune-mediated disorders. In research settings, perturbing GSDMA supports mechanistic studies of inflammasome-linked pathways, epithelial differentiation, and stress-triggered cell death phenotypes.
gasdermin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GSDMA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GSDMA. 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 GSDMA 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 GSDMA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.