CD47 Double Nickase Plasmid (m): sc-421180-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD47 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
- CD47 Double Nickase Plasmid (m) and CD47 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cd47. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD47 Antibody (MIAP301): sc-12731
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD47 Double Nickase Plasmid (m) | sc-421180-NIC | 20 µg | $410.00 | |||
CD47 Double Nickase Plasmid (m2) | sc-421180-NIC-2 | 20 µg | $410.00 |
Cd47 encodes CD47, a broadly expressed immunoglobulin superfamily receptor that functions as a “don’t eat me” signal through binding to SIRPα on macrophages, thereby modulating phagocytosis and innate immune checkpoints. CD47 also interacts with thrombospondin-1 to influence integrin signaling, cell adhesion, migration, and nitric oxide–dependent vascular responses. In mouse tissues, CD47 contributes to homeostatic clearance of cells, regulation of inflammatory signaling, and shaping of tumor–immune interactions. Dysregulated CD47 signaling has been implicated in immune evasion, chronic inflammation, and altered hematopoietic and vascular biology, making it a relevant node for mechanistic studies of immune surveillance pathways.
CD47 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cd47 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cd47. 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 Cd47 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 Cd47-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.