IFI-204 Double Nickase Plasmid (m): sc-421033-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFI-204 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
- IFI-204 Double Nickase Plasmid (m) and IFI-204 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ifi204. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFI-204 Double Nickase Plasmid (m) | sc-421033-NIC | 20 µg | $410.00 | |||
IFI-204 Double Nickase Plasmid (m2) | sc-421033-NIC-2 | 20 µg | $410.00 |
Ifi204 encodes IFI-204, a murine interferon-inducible member of the p200 family that functions as a nucleic acid–responsive regulator of innate immunity. IFI-204 participates in sensing cytosolic DNA and modulating interferon-stimulated gene programs, shaping downstream signaling through STING–TBK1–IRF3 and related inflammatory transcriptional networks. Beyond pathogen response, IFI-204 has been linked to control of cell-cycle progression, differentiation, and senescence-associated programs in immune and stromal contexts. Dysregulated IFI-204 activity is therefore relevant to models of autoinflammation, antiviral defense, and tumor-associated immune signaling where interferon pathways and DNA sensing influence disease phenotypes.
IFI-204 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ifi204 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ifi204. 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 Ifi204 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 Ifi204-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.