NERF Double Nickase Plasmid (m): sc-427352-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NERF 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
- NERF Double Nickase Plasmid (m) and NERF Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Elf2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NERF Double Nickase Plasmid (m) | sc-427352-NIC | 20 µg | $410.00 |
Elf2 encodes NERF (new Ets-related factor), a member of the ETS family of transcription factors that binds ETS motifs to regulate cell type–specific gene expression programs. In mouse, NERF contributes to hematopoietic and lymphoid lineage biology by coordinating transcriptional networks involved in differentiation, activation, and immune signaling, including pathways downstream of cytokine and antigen receptor cues. Through its role in controlling genes linked to proliferation and survival, altered ELF2/NERF activity is frequently studied in contexts of dysregulated hematopoiesis and immune dysfunction. These properties make Elf2 a useful target for mechanistic studies of transcriptional control, lineage commitment, and stress-responsive gene regulation.
NERF Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Elf2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Elf2. 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 Elf2 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 Elf2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.