Slfn12 Double Nickase Plasmid (h): sc-404339-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Slfn12 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
- Slfn12 Double Nickase Plasmid (h) and Slfn12 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLFN12. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Slfn12 Double Nickase Plasmid (h) | sc-404339-NIC | 20 µg | $410.00 | |||
Slfn12 Double Nickase Plasmid (h2) | sc-404339-NIC-2 | 20 µg | $410.00 |
Human SLFN12 encodes Schlafen family member 12 (Slfn12), a cytosolic protein implicated in regulation of cellular differentiation and post-transcriptional control of gene expression. SLFN proteins are broadly linked to modulation of RNA metabolism and translational programs that shape proliferation and stress-adaptive responses, positioning SLFN12 at the interface of growth control and cell-state transitions. Altered SLFN12 activity and expression patterns have been examined in contexts where differentiation and cell-cycle balance are perturbed, supporting its relevance to mechanistic studies of dysregulated growth and lineage commitment in disease-associated models. As part of the wider interferon-responsive Schlafen network, SLFN12 is also used to probe how innate immune signaling intersects with fundamental gene expression control.
Slfn12 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLFN12 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLFN12. 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 SLFN12 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 SLFN12-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.