C4a Double Nickase Plasmid (h): sc-402428-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C4a 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
- C4a Double Nickase Plasmid (h) and C4a Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C4A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C4a Double Nickase Plasmid (h) | sc-402428-NIC | 20 µg | $410.00 | |||
C4a Double Nickase Plasmid (h2) | sc-402428-NIC-2 | 20 µg | $410.00 |
Complement component 4A (C4A) encodes C4a, a proteolytic fragment generated during activation of the classical and lectin complement pathways. C4a is released upon cleavage of C4 and contributes to innate immune signaling by modulating local inflammatory responses in concert with downstream complement effector mechanisms, including C3 convertase formation and opsonization cascades. Variation in C4A gene copy number and complement activity has been associated with immune dysregulation, including autoimmunity and neuroinflammatory processes, making C4A a key locus for mechanistic studies. In cellular models, perturbing C4A helps define how complement-mediated signaling intersects with antigen handling, cytokine networks, and tissue homeostasis.
C4a Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C4A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C4A. 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 C4A 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 C4A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.