G-CSF Double Nickase Plasmid (m): sc-419844-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- G-CSF 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
- G-CSF Double Nickase Plasmid (m) and G-CSF Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Csf3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
G-CSF Double Nickase Plasmid (m) | sc-419844-NIC | 20 µg | $410.00 | |||
G-CSF Double Nickase Plasmid (m2) | sc-419844-NIC-2 | 20 µg | $410.00 |
Colony stimulating factor 3 (Csf3) encodes granulocyte colony-stimulating factor (G-CSF), a secreted cytokine that regulates granulopoiesis and neutrophil mobilization from the bone marrow. In mouse hematopoietic and stromal contexts, G-CSF signals primarily through the CSF3R receptor to engage JAK/STAT, MAPK/ERK, and PI3K/AKT pathways, coordinating myeloid progenitor proliferation, differentiation, and survival. This axis shapes innate immune homeostasis and inflammatory responses, and altered signaling is commonly studied in models of neutropenia, infection susceptibility, and dysregulated myelopoiesis. Csf3 is also used to interrogate neutrophil-driven pathology in inflammatory disease models where cytokine networks and myeloid trafficking are mechanistically important.
G-CSF Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Csf3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Csf3. 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 Csf3 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 Csf3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.