C1r Double Nickase Plasmid (h): sc-405842-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C1r 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
- C1r Double Nickase Plasmid (h) and C1r Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C1R. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: C1r Antibody (F-7): sc-514105
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C1r Double Nickase Plasmid (h) | sc-405842-NIC | 20 µg | $410.00 | |||
C1r Double Nickase Plasmid (h2) | sc-405842-NIC-2 | 20 µg | $410.00 |
C1R encodes complement C1r, a serine protease that forms the C1 complex with C1q and C1s to initiate the classical complement cascade. Upon activation, C1r cleaves and activates C1s, driving downstream cleavage of C4 and C2 and promoting opsonization and inflammatory signaling. C1r function connects innate immune surveillance with clearance of immune complexes and modulation of cytokine networks. Dysregulated C1R activity and classical pathway imbalance have been associated with complement-mediated inflammatory phenotypes and immune-complex–related tissue injury, supporting its use as a mechanistic target in immunology research.
C1r Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C1R locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C1R. 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 C1R 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 C1R-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.