C7 Double Nickase Plasmid (h): sc-404773-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C7 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
- C7 Double Nickase Plasmid (h) and C7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C7 Double Nickase Plasmid (h) | sc-404773-NIC | 20 µg | $410.00 | |||
C7 Double Nickase Plasmid (h2) | sc-404773-NIC-2 | 20 µg | $410.00 |
Complement component C7 encodes a terminal pathway protein of the complement system that participates in membrane attack complex (MAC) assembly by binding the C5b-6 complex and promoting insertion of C8 and polymerization of C9 on target membranes. This activity supports innate immune defense and inflammatory clearance mechanisms through the classical, lectin, and alternative complement pathways converging at C5 activation. Dysregulated complement activation and altered MAC formation have been implicated in immune-mediated tissue injury and susceptibility to certain infections, making C7 a useful node for studying complement effector function. C7 also provides a tractable readout for investigating extracellular immune signaling, opsonophagocytic responses, and crosstalk with cytokine-driven inflammation.
C7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C7. 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 C7 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 C7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.