IRGC1 Double Nickase Plasmid (h): sc-412702-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRGC1 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
- IRGC1 Double Nickase Plasmid (h) and IRGC1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IRGC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRGC1 Double Nickase Plasmid (h) | sc-412702-NIC | 20 µg | $410.00 |
IRGC (immunity-related GTPase family, member C) encodes IRGC1, a small interferon-inducible GTPase implicated in cell-intrinsic defense programs and dynamic remodeling of intracellular membranes. As part of the broader IRG/GBTPase network, IRGC1 is thought to interface with innate immune signaling, vesicle trafficking, and autophagy-linked processes that influence pathogen restriction and inflammatory homeostasis. Altered regulation of interferon-stimulated GTPases has been associated with dysregulated cytokine signaling and immune-mediated tissue pathology, making IRGC a useful locus for mechanistic studies of interferon-responsive pathways. Human IRGC1 is therefore of interest for dissecting GTPase-dependent steps in host defense and cellular stress responses.
IRGC1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IRGC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IRGC. 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 IRGC 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 IRGC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.