IDS Double Nickase Plasmid (h): sc-404268-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IDS 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
- IDS Double Nickase Plasmid (h) and IDS Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IDS. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IDS Antibody (B-5): sc-365047
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IDS Double Nickase Plasmid (h) | sc-404268-NIC | 20 µg | $410.00 | |||
IDS Double Nickase Plasmid (h2) | sc-404268-NIC-2 | 20 µg | $410.00 |
Human IDS encodes iduronate 2-sulfatase, a lysosomal sulfatase required for stepwise degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate. By catalyzing hydrolysis of 2-O-sulfate groups on iduronic acid residues, IDS supports lysosome-mediated macromolecule turnover and interfaces with broader endolysosomal trafficking and autophagy-associated processes. Disruption of IDS activity leads to lysosomal storage with secondary effects on cellular stress responses, extracellular matrix remodeling, and inflammatory signaling networks. IDS is therefore widely studied in the context of glycosaminoglycan catabolism, lysosomal biology, and genotype–phenotype relationships in mucopolysaccharidosis type II (Hunter syndrome) research models.
IDS Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IDS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IDS. 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 IDS 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 IDS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.