C3 Double Nickase Plasmid (m): sc-419391-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C3 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
- C3 Double Nickase Plasmid (m) and C3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting C3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: C3 Antibody (B-9): sc-28294
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C3 Double Nickase Plasmid (m) | sc-419391-NIC | 20 µg | $410.00 |
Mouse C3 encodes complement component 3, the central hub of the complement cascade that is cleaved into C3a and C3b to amplify innate immune responses. C3b deposition drives opsonization and promotes immune complex clearance, while downstream signaling supports C5 convertase formation and membrane attack complex assembly. Through crosstalk with inflammatory cytokine networks and phagocyte activation, C3 influences tissue homeostasis and barrier defense. Dysregulated C3 activity is implicated in inflammatory and autoimmune processes, susceptibility to infection, and complement-mediated tissue injury relevant to neuroinflammation, kidney disease models, and metabolic inflammation.
C3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the C3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C3. 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 C3 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 C3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.