IRGM Double Nickase Plasmid (h): sc-407889-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRGM 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
- IRGM Double Nickase Plasmid (h) and IRGM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IRGM. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRGM Double Nickase Plasmid (h) | sc-407889-NIC | 20 µg | $410.00 | |||
IRGM Double Nickase Plasmid (h2) | sc-407889-NIC-2 | 20 µg | $410.00 |
IRGM (immunity-related GTPase M) is a human interferon-inducible GTPase that coordinates selective autophagy and innate immune defense, with prominent roles in xenophagy of intracellular pathogens and regulation of autophagosome formation and maturation. It interfaces with autophagy machinery and membrane trafficking pathways to influence clearance of bacteria and modulation of inflammatory signaling. Genetic and functional studies have linked IRGM-associated dysregulation of autophagy to altered host–microbe interactions and chronic inflammatory phenotypes, including susceptibility signals reported in inflammatory bowel disease and related mucosal immune disorders. As a node connecting autophagy, pathogen sensing, and cytokine responses, IRGM is frequently investigated in studies of cellular stress adaptation, antimicrobial restriction, and inflammatory homeostasis.
IRGM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IRGM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IRGM. 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 IRGM 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 IRGM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.