CD35 Double Nickase Plasmid (h): sc-401210-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD35 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
- CD35 Double Nickase Plasmid (h) and CD35 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD35 Antibody (E-11): sc-7308
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD35 Double Nickase Plasmid (h) | sc-401210-NIC | 20 µg | $410.00 | |||
CD35 Double Nickase Plasmid (h2) | sc-401210-NIC-2 | 20 µg | $410.00 |
CR1 encodes complement receptor 1 (CD35), a cell-surface glycoprotein that binds C3b/C4b to promote clearance of immune complexes and regulate complement activation on host cells. CD35 functions in innate immune surveillance by supporting opsonization, phagocytosis, and limiting excessive complement-mediated inflammation, with prominent roles on erythrocytes, leukocytes, and antigen-presenting cells. Through these interactions, CR1 influences B cell responses and antigen handling in lymphoid tissues, linking complement biology to adaptive immune modulation. Genetic and expression variation in CR1 has been associated with immune-complex–driven pathology and inflammatory disease contexts, making it a relevant target for mechanistic studies of complement regulation.
CD35 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CR1. 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 CR1 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 CR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.