C4b Double Nickase Plasmid (h): sc-416372-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C4b 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
- C4b Double Nickase Plasmid (h) and C4b Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C4B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C4b Double Nickase Plasmid (h) | sc-416372-NIC | 20 µg | $410.00 | |||
C4b Double Nickase Plasmid (h2) | sc-416372-NIC-2 | 20 µg | $410.00 |
Complement component 4B (C4B) encodes C4b, a central opsonin generated during activation of the classical and lectin complement pathways. Following cleavage, C4b covalently attaches to target surfaces and participates in C3 convertase formation, amplifying complement-mediated immune surveillance, immune complex clearance, and crosstalk with inflammatory signaling. Variation in C4 gene copy number and sequence is linked to altered complement activity and has been associated with susceptibility to autoimmune and inflammatory disorders, including systemic autoimmunity and infection-related immune dysregulation. As a result, C4B is frequently studied in pathways governing humoral immunity, complement consumption, and tissue inflammation.
C4b Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C4B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C4B. 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 C4B 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 C4B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.