Neurofibromin Double Nickase Plasmid (m): sc-421861-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Neurofibromin 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
- Neurofibromin Double Nickase Plasmid (m) and Neurofibromin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nf1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Neurofibromin Antibody (H-12): sc-376886
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Neurofibromin Double Nickase Plasmid (m) | sc-421861-NIC | 20 µg | $410.00 | |||
Neurofibromin Double Nickase Plasmid (m2) | sc-421861-NIC-2 | 20 µg | $410.00 |
Mouse Nf1 encodes neurofibromin, a Ras GTPase-activating protein that downregulates RAS signaling by accelerating conversion of active Ras-GTP to Ras-GDP. Through modulation of RAF–MEK–ERK and PI3K–AKT–mTOR pathways, neurofibromin influences proliferation, differentiation, survival, and neuronal/glial development. Nf1 also impacts cytoskeletal organization and cAMP-dependent signaling, linking growth factor cues to cell fate decisions. Dysregulation of NF1 function is associated with aberrant Ras pathway activation and is widely studied in contexts of tumor predisposition biology and neurodevelopmental phenotypes in mouse models.
Neurofibromin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nf1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nf1. 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 Nf1 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 Nf1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.