M-CSF Double Nickase Plasmid (h): sc-401339-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- M-CSF 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
- M-CSF Double Nickase Plasmid (h) and M-CSF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CSF1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: M-CSF Antibody (D-4): sc-365779
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
M-CSF Double Nickase Plasmid (h) | sc-401339-NIC | 20 µg | $410.00 | |||
M-CSF Double Nickase Plasmid (h2) | sc-401339-NIC-2 | 20 µg | $410.00 |
CSF1 encodes macrophage colony-stimulating factor (M-CSF), a secreted cytokine that governs monocyte survival, proliferation, and differentiation into macrophages and osteoclasts. M-CSF signals primarily through CSF1R to activate PI3K–AKT, MAPK/ERK, and JAK/STAT pathways, shaping innate immune homeostasis, phagocytic function, and tissue remodeling. Altered CSF1–CSF1R signaling is linked to dysregulated inflammatory responses and aberrant macrophage polarization, with downstream effects on bone turnover and tumor–stroma crosstalk in the microenvironment. As a regulator of myeloid lineage biology, M-CSF is frequently studied in pathways controlling osteoclastogenesis, wound repair, and cytokine-driven differentiation programs.
M-CSF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CSF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CSF1. 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 CSF1 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 CSF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.