C2 Double Nickase Plasmid (h): sc-405804-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C2 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
- C2 Double Nickase Plasmid (h) and C2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: C2 Antibody (E-7): sc-373809
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C2 Double Nickase Plasmid (h) | sc-405804-NIC | 20 µg | $410.00 | |||
C2 Double Nickase Plasmid (h2) | sc-405804-NIC-2 | 20 µg | $410.00 |
Human C2 encodes complement component C2, a serine protease zymogen that is cleaved to form C2a, a catalytic subunit of the classical and lectin pathway C3 convertase (C4b2a). Through these pathways, C2 supports opsonization, immune complex clearance, and amplification of downstream complement signaling that links innate and adaptive immunity. Genetic deficiency or dysregulation of C2 is associated with altered susceptibility to infection and immune-complex–mediated inflammation, and complement pathway activity is implicated in autoimmune and inflammatory disease biology. Experimental modulation of C2 is therefore relevant for dissecting complement activation, inflammatory signaling, and host–pathogen interactions in human cell models.
C2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C2. 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 C2 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 C2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.