Slfn5 Double Nickase Plasmid (m): sc-435875-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Slfn5 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
- Slfn5 Double Nickase Plasmid (m) and Slfn5 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slfn5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Slfn5 Double Nickase Plasmid (m) | sc-435875-NIC | 20 µg | $410.00 | |||
Slfn5 Double Nickase Plasmid (m2) | sc-435875-NIC-2 | 20 µg | $410.00 |
Slfn5 (schlafen family member 5) is a mouse interferon-stimulated gene implicated in regulating immune cell activation and differentiation, linking innate immune signaling to transcriptional control programs. As part of the Schlafen family, Slfn5 is commonly studied in the context of type I interferon/JAK–STAT pathway responses and broader antiviral and inflammatory signaling networks that shape cellular proliferation and gene expression. Altered Schlafen-family activity has been associated with dysregulated immune responses and inflammatory phenotypes, making Slfn5 a relevant target for mechanistic studies of interferon-driven transcriptional states. In biomedical research, Slfn5 is used to probe how cytokine cues remodel chromatin and transcription to influence immune homeostasis and disease-relevant inflammation models.
Slfn5 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slfn5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slfn5. 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 Slfn5 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 Slfn5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.