Slfn13 Double Nickase Plasmid (h): sc-414596-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Slfn13 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
- Slfn13 Double Nickase Plasmid (h) and Slfn13 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLFN13. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Slfn13 Double Nickase Plasmid (h) | sc-414596-NIC | 20 µg | $410.00 | |||
Slfn13 Double Nickase Plasmid (h2) | sc-414596-NIC-2 | 20 µg | $410.00 |
SLFN13 (Schlafen family member 13) encodes Slfn13, a putative RNA-directed endoribonuclease implicated in post-transcriptional control of gene expression and cellular innate immune programs. As part of the interferon-stimulated gene network, SLFN13 is associated with regulation of RNA stability/translation, modulation of stress responses, and control of proliferation and differentiation states. Schlafen proteins are frequently linked to antiviral restriction and immune signaling pathways, including interferon and inflammatory transcriptional programs. Dysregulated SLFN family activity has been observed in contexts of immune dysfunction and cancer biology, supporting the use of SLFN13 perturbation to probe RNA metabolism and interferon-linked phenotypes.
Slfn13 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLFN13 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLFN13. 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 SLFN13 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 SLFN13-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.